Anoikis: APOPTOSIS triggered by loss of contact with the EXTRACELLULAR MATRIX.Cell Adhesion: Adherence of cells to surfaces or to other cells.Cell Line, Tumor: A cell line derived from cultured tumor cells.Extracellular Matrix: A meshwork-like substance found within the extracellular space and in association with the basement membrane of the cell surface. It promotes cellular proliferation and provides a supporting structure to which cells or cell lysates in culture dishes adhere.Digitoxin: A cardiac glycoside sometimes used in place of DIGOXIN. It has a longer half-life than digoxin; toxic effects, which are similar to those of digoxin, are longer lasting. (From Martindale, The Extra Pharmacopoeia, 30th ed, p665)Carcinoma, Non-Small-Cell Lung: A heterogeneous aggregate of at least three distinct histological types of lung cancer, including SQUAMOUS CELL CARCINOMA; ADENOCARCINOMA; and LARGE CELL CARCINOMA. They are dealt with collectively because of their shared treatment strategy.Lung Neoplasms: Tumors or cancer of the LUNG.Monosaccharides: Simple sugars, carbohydrates which cannot be decomposed by hydrolysis. They are colorless crystalline substances with a sweet taste and have the same general formula CnH2nOn. (From Dorland, 28th ed)Neoplasm Metastasis: The transfer of a neoplasm from one organ or part of the body to another remote from the primary site.Metformin: A biguanide hypoglycemic agent used in the treatment of non-insulin-dependent diabetes mellitus not responding to dietary modification. Metformin improves glycemic control by improving insulin sensitivity and decreasing intestinal absorption of glucose. (From Martindale, The Extra Pharmacopoeia, 30th ed, p289)Hypoglycemic Agents: Substances which lower blood glucose levels.Glucose: A primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used therapeutically in fluid and nutrient replacement.Cell Proliferation: All of the processes involved in increasing CELL NUMBER including CELL DIVISION.Carcinoma, Squamous Cell: A carcinoma derived from stratified SQUAMOUS EPITHELIAL CELLS. It may also occur in sites where glandular or columnar epithelium is normally present. (From Stedman, 25th ed)Papilloma: A circumscribed benign epithelial tumor projecting from the surrounding surface; more precisely, a benign epithelial neoplasm consisting of villous or arborescent outgrowths of fibrovascular stroma covered by neoplastic cells. (Stedman, 25th ed)Stomach Neoplasms: Tumors or cancer of the STOMACH.Genetic Vectors: DNA molecules capable of autonomous replication within a host cell and into which other DNA sequences can be inserted and thus amplified. Many are derived from PLASMIDS; BACTERIOPHAGES; or VIRUSES. They are used for transporting foreign genes into recipient cells. Genetic vectors possess a functional replicator site and contain GENETIC MARKERS to facilitate their selective recognition.Hypoxia-Inducible Factor 1, alpha Subunit: Hypoxia-inducible factor 1, alpha subunit is a basic helix-loop-helix transcription factor that is regulated by OXYGEN availability and is targeted for degradation by VHL TUMOR SUPPRESSOR PROTEIN.Oligonucleotides, Antisense: Short fragments of DNA or RNA that are used to alter the function of target RNAs or DNAs to which they hybridize.Lentivirus: A genus of the family RETROVIRIDAE consisting of non-oncogenic retroviruses that produce multi-organ diseases characterized by long incubation periods and persistent infection. Lentiviruses are unique in that they contain open reading frames (ORFs) between the pol and env genes and in the 3' env region. Five serogroups are recognized, reflecting the mammalian hosts with which they are associated. HIV-1 is the type species.Receptor, trkB: A protein-tyrosine kinase receptor that is specific for BRAIN-DERIVED NEUROTROPHIC FACTOR; NEUROTROPHIN 3; neurotrophin 4 and neurotrophin 5. It is widely expressed in nervous tissue and plays a role in mediating the effects of neurotrophins on growth and differentiation of neuronal cells.Phosphatidylinositols: Derivatives of phosphatidic acids in which the phosphoric acid is bound in ester linkage to the hexahydroxy alcohol, myo-inositol. Complete hydrolysis yields 1 mole of glycerol, phosphoric acid, myo-inositol, and 2 moles of fatty acids.Brain-Derived Neurotrophic Factor: A member of the nerve growth factor family of trophic factors. In the brain BDNF has a trophic action on retinal, cholinergic, and dopaminergic neurons, and in the peripheral nervous system it acts on both motor and sensory neurons. (From Kendrew, The Encyclopedia of Molecular Biology, 1994)Kidney Neoplasms: Tumors or cancers of the KIDNEY.Carcinoma, Renal Cell: A heterogeneous group of sporadic or hereditary carcinoma derived from cells of the KIDNEYS. There are several subtypes including the clear cells, the papillary, the chromophobe, the collecting duct, the spindle cells (sarcomatoid), or mixed cell-type carcinoma.AnilidesBenzenesulfonates: Organic salts and esters of benzenesulfonic acid.Niacinamide: An important compound functioning as a component of the coenzyme NAD. Its primary significance is in the prevention and/or cure of blacktongue and PELLAGRA. Most animals cannot manufacture this compound in amounts sufficient to prevent nutritional deficiency and it therefore must be supplemented through dietary intake.Phenylurea Compounds: Compounds that include the amino-N-phenylamide structure.QuinolinesOvarian Neoplasms: Tumors or cancer of the OVARY. These neoplasms can be benign or malignant. They are classified according to the tissue of origin, such as the surface EPITHELIUM, the stromal endocrine cells, and the totipotent GERM CELLS.Antigens, CD147: A widely distributed cell surface transmembrane glycoprotein that stimulates the synthesis of MATRIX METALLOPROTEINASES. It is found at high levels on the surface of malignant NEOPLASMS and may play a role as a mediator of malignant cell behavior.Matrix Metalloproteinases: A family of zinc-dependent metalloendopeptidases that is involved in the degradation of EXTRACELLULAR MATRIX components.Matrix Metalloproteinase 2: A secreted endopeptidase homologous with INTERSTITIAL COLLAGENASE, but which possesses an additional fibronectin-like domain.Matrix Metalloproteinase 9: An endopeptidase that is structurally similar to MATRIX METALLOPROTEINASE 2. It degrades GELATIN types I and V; COLLAGEN TYPE IV; and COLLAGEN TYPE V.Matrix Metalloproteinase 1: A member of the metalloproteinase family of enzymes that is principally responsible for cleaving FIBRILLAR COLLAGEN. It can degrade interstitial collagens, types I, II and III.Hydrocarbons, IodinatedNerve Growth Factor: NERVE GROWTH FACTOR is the first of a series of neurotrophic factors that were found to influence the growth and differentiation of sympathetic and sensory neurons. It is comprised of alpha, beta, and gamma subunits. The beta subunit is responsible for its growth stimulating activity.Nerve Growth Factors: Factors which enhance the growth potentialities of sensory and sympathetic nerve cells.Seeds: The encapsulated embryos of flowering plants. They are used as is or for animal feed because of the high content of concentrated nutrients like starches, proteins, and fats. Rapeseed, cottonseed, and sunflower seed are also produced for the oils (fats) they yield.Receptor, Nerve Growth Factor: A low affinity receptor that binds NERVE GROWTH FACTOR; BRAIN-DERIVED NEUROTROPHIC FACTOR; NEUROTROPHIN 3; and neurotrophin 4.MicroRNAs: Small double-stranded, non-protein coding RNAs, 21-25 nucleotides in length generated from single-stranded microRNA gene transcripts by the same RIBONUCLEASE III, Dicer, that produces small interfering RNAs (RNA, SMALL INTERFERING). They become part of the RNA-INDUCED SILENCING COMPLEX and repress the translation (TRANSLATION, GENETIC) of target RNA by binding to homologous 3'UTR region as an imperfect match. The small temporal RNAs (stRNAs), let-7 and lin-4, from C. elegans, are the first 2 miRNAs discovered, and are from a class of miRNAs involved in developmental timing.Ovary: The reproductive organ (GONADS) in female animals. In vertebrates, the ovary contains two functional parts: the OVARIAN FOLLICLE for the production of female germ cells (OOGENESIS); and the endocrine cells (GRANULOSA CELLS; THECA CELLS; and LUTEAL CELLS) for the production of ESTROGENS and PROGESTERONE.Neoplasms: New abnormal growth of tissue. Malignant neoplasms show a greater degree of anaplasia and have the properties of invasion and metastasis, compared to benign neoplasms.Epithelial Cells: Cells that line the inner and outer surfaces of the body by forming cellular layers (EPITHELIUM) or masses. Epithelial cells lining the SKIN; the MOUTH; the NOSE; and the ANAL CANAL derive from ectoderm; those lining the RESPIRATORY SYSTEM and the DIGESTIVE SYSTEM derive from endoderm; others (CARDIOVASCULAR SYSTEM and LYMPHATIC SYSTEM) derive from mesoderm. Epithelial cells can be classified mainly by cell shape and function into squamous, glandular and transitional epithelial cells.Neoplasms, Glandular and Epithelial: Neoplasms composed of glandular tissue, an aggregation of epithelial cells that elaborate secretions, and of any type of epithelium itself. The concept does not refer to neoplasms located in the various glands or in epithelial tissue.Paclitaxel: A cyclodecane isolated from the bark of the Pacific yew tree, TAXUS BREVIFOLIA. It stabilizes MICROTUBULES in their polymerized form leading to cell death.Receptors, Eicosanoid: Cell surface proteins that bind eicosanoids with high affinity and trigger intracellular changes influencing the behavior of cells. Among the eicosanoid receptors are receptors for the prostaglandins, thromboxanes, and leukotrienes.Hydroxyeicosatetraenoic Acids: Eicosatetraenoic acids substituted in any position by one or more hydroxy groups. They are important intermediates in a series of biosynthetic processes leading from arachidonic acid to a number of biologically active compounds such as prostaglandins, thromboxanes, and leukotrienes.Encyclopedias as Topic: Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)12-Hydroxy-5,8,10,14-eicosatetraenoic Acid: A lipoxygenase metabolite of ARACHIDONIC ACID. It is a highly selective ligand used to label mu-opioid receptors in both membranes and tissue sections. The 12-S-HETE analog has been reported to augment tumor cell metastatic potential through activation of protein kinase C. (J Pharmacol Exp Ther 1995; 274(3):1545-51; J Natl Cancer Inst 1994; 86(15):1145-51)Arachidonate 12-Lipoxygenase: An enzyme that catalyzes the oxidation of arachidonic acid to yield 12-hydroperoxyarachidonate (12-HPETE) which is itself rapidly converted by a peroxidase to 12-hydroxy-5,8,10,14-eicosatetraenoate (12-HETE). The 12-hydroperoxides are preferentially formed in PLATELETS.Arachidonate Lipoxygenases: Enzymes catalyzing the oxidation of arachidonic acid to hydroperoxyarachidonates. These products are then rapidly converted by a peroxidase to hydroxyeicosatetraenoic acids. The positional specificity of the enzyme reaction varies from tissue to tissue. The final lipoxygenase pathway leads to the leukotrienes. EC 1.13.11.- .Arachidonic Acid: An unsaturated, essential fatty acid. It is found in animal and human fat as well as in the liver, brain, and glandular organs, and is a constituent of animal phosphatides. It is formed by the synthesis from dietary linoleic acid and is a precursor in the biosynthesis of prostaglandins, thromboxanes, and leukotrienes.

Matrix attachment regulates Fas-induced apoptosis in endothelial cells: a role for c-flip and implications for anoikis. (1/360)

Survival of endothelial cells is critical for cellular processes such as angiogenesis. Cell attachment to extracellular matrix inhibits apoptosis in endothelial cells both in vitro and in vivo, but the molecular mechanisms underlying matrix-induced survival signals or detachment-induced apoptotic signals are unknown. We demonstrate here that matrix attachment is an efficient regulator of Fas-mediated apoptosis in endothelial cells. Thus, matrix attachment protects cells from Fas-induced apoptosis, whereas matrix detachment results in susceptibility to Fas-mediated cell death. Matrix attachment modulates Fas-mediated apoptosis at two different levels: by regulating the expression level of Fas, and by regulating the expression level of c-Flip, an endogenous antagonist of caspase-8. The extracellular signal-regulated kinase (Erk) cascade functions as a survival pathway in adherent cells by regulating c-Flip expression. We further show that detachment-induced cell death, or anoikis, itself results from activation of the Fas pathway by its ligand, Fas-L. Fas-L/Fas interaction, Fas-FADD complex formation, and caspase-8 activation precede the bulk of anoikis in endothelial cells, and inhibition of any of these events blocks anoikis. These studies identify matrix attachment as a survival factor against death receptor-mediated apoptosis and provide a molecular mechanism for anoikis and previously observed Fas resistance in endothelial cells.  (+info)

Global effects of anchorage on gene expression during mammary carcinoma cell growth reveal role of tumor necrosis factor-related apoptosis-inducing ligand in anoikis. (2/360)

Anchorage-independent growth is a hallmark of tumor cells. We compared gene expression profiles of anchored and nonanchored human mammary carcinoma cells to study this phenomenon. In this study, we show that anchorage had striking effects on cell growth and morphology but altered transcript levels from a limited number of genes. Only about 1% of mRNA transcripts detected in these cells was altered by anchorage. These include genes related to amino acid and polyamine metabolism, apoptosis, ion channels, cytoskeletal and stress proteins, transcription factors, and growth factors. Some of these may be crucial for the survival of transformed cells. For example, clusterin and the tumor necrosis factor-related apoptosis inducing ligand (TRAIL) were suppressed by anchorage, which could help prevent programmed cell death of these tumor cells. In addition to suppressing TRAIL expression, anchorage also decreased the susceptibility of these tumor cells to TRAIL-induced apoptosis as determined by poly(ADP-ribose) phosphorylase cleavage, annexin-V binding (P < 0.01), and cell cycle analysis (P < 0.0001). These data may help explain mechanisms by which anchorage prevents apoptosis of cells that would otherwise experience anoikis. Thus, genes found to be altered by this analysis could serve as potential targets for anticancer therapy. These findings suggest that TRAIL may be used as a means to target circulating epithelial tumor cells before their attachment and colonization at new sites.  (+info)

Anoikis and metastatic potential of cloudman S91 melanoma cells. (3/360)

Anoikis is a form of apoptosis induced in normal cells as a result of loss of their adhesion to substrate. In the present study, we have tested whether tumor cells are also sensitive to anoikis and whether selection of tumor cells for resistance to anoikis could increase their metastatic ability. In vitro cultured Cloudman S91 melanoma cells are strongly adherent to the plastic. Prevention of their adherence by rocking or by covering culture plates with polyhydroxyethylmethacrylate resulted in induction of anoikis and death of almost all cells. Their death was prevented in the presence of caspase inhibitor Z-Val-Ala-Asp-fluoromethyl ketone. To select anoikis-resistant cells, S91 cells floating in the culture medium were sequentially isolated and transferred for seven generations. As a result, a new subline of S91 cells capable of growing in free cell suspension was selected. These S91 nonadherent (S91Nadh) cells were completely resistant to anoikis and manifested higher metastatic ability than S91Adh cells. Anoikis resistance of S91Nadh cells was not attributable to their resistance to other apoptotic signals in vitro, and they showed no increase in their survival in vivo in the lungs after i.v. inoculation. Increased metastatic potential of the anoikis-resistant S91Nadh cells was associated with various phenotypic changes, including increased proliferation and loss of VLA-4 integrin expression because of down-regulation of the VLA-49alpha (CLD49d) gene. In parallel, they showed a reduction in homotypic aggregation and binding to endothelial cells, increased Matrigel invasiveness, and decreased matrix metalloproteinase-2 and matrix metalloproteinase-9 activity that paralleled up-regulation of the TIMP-1 gene. S91Nadh cells also manifested changes in cell surface carbohydrates, such as appearance of alpha-galactosyl epitopes as a result of up-regulation of the alpha1,3-galactosyltransferase gene and concomitant reduction in cell membrane sialylation. Thus, selection of S91 melanoma cells for anoikis resistance resulted in an increase in their metastatic potential in parallel with multiple alterations in their phenotypic properties.  (+info)

Tyrosine kinase-dependent, phosphatidylinositol 3'-kinase, and mitogen-activated protein kinase-independent signaling pathways prevent lung adenocarcinoma cells from anoikis. (4/360)

Normal epithelial cells are anchorage-dependent. Detachment of normal epithelial cells from their substratum causes apoptosis, termed anoikis. Malignant tumor cells, however, can survive and proliferate independent of anchorage. To understand the molecular basis of tumor cell anchorage independence, we investigated the role of tyrosine kinases and their downstream signaling pathways in anoikis resistance of human lung adenocarcinoma cells. Four of the five lung adenocarcinoma cell lines analyzed are resistant to anoikis. Tyrosine kinase inhibitor genistein rendered three of them sensitive to anoikis. Although cell detachment induced rapid protein tyrosine dephosphorylation in Madin-Darby canine kidney cells, a nontransformed epithelial cell line, tyrosine phosphorylation of several proteins in the tumor cells is anchorage-independent. Similarly, phosphorylation of Akt and mitogen-activated protein kinase, two signaling proteins downstream of tyrosine kinases, was decreased in Madin-Darby canine kidney cells but increased in some of the tumor cells upon cell detachment. Inhibition of phosphorylation of the two proteins, however, did not induce anoikis in the tumor cells. Specific inhibitors to several known tyrosine kinases also failed to induce anoikis in these cells. These data suggest the existence of tyrosine kinase-dependent phosphatidylinositol 3'-kinase and mitogen-activated protein kinase-independent signaling pathways that function to regulate cell survival and death. Alteration in these pathways may count for the anchorage-independent survival of the lung adenocarcinoma cells and other malignant tumor cells.  (+info)

Caspases as key executors of methyl selenium-induced apoptosis (anoikis) of DU-145 prostate cancer cells. (5/360)

Apoptosis induction may be a mechanism mediating the anticancer activity of selenium. Our earlier work indicated that distinct cell death pathways are likely involved in apoptosis induced by the CH3SeH and the hydrogen selenide pools of selenium metabolites. To explore the role of caspases in cancer cell apoptosis induced by selenium, we examined the involvement of these molecules in the death of the DU-145 human prostate carcinoma cells induced by methylseleninic acid (MSeA), a novel penultimate precursor of the putative critical anticancer metabolite CH3SeH. Sodium selenite, a representative of the genotoxic selenium pool, was used as a reference for comparison. The results show that MSeA-induced apoptosis was accompanied by the activation of multiple caspases (caspase-3, -7, -8, and -9), mitochondrial release of cytochrome c (CC), poly(ADP-ribose) polymerase (PARP) cleavage, and DNA fragmentation. In contrast, selenite-induced apoptotic DNA fragmentation was observed in the absence of these changes, but was associated with the phosphorylation of c-Jun-NH2-terminal kinase 1/2 and p38 mitogen-activated protein kinase/stress-activated protein kinase 2. A general caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp-(OMe) fluoromethyl ketone, blocked MSeA-induced cleavage of procaspases and PARP, CC release, and DNA nucleosomal fragmentation, but did not prevent cell detachment. Furthermore, PARP cleavage and caspase activation were confined exclusively to detached cells, indicating that MSeA induction of cell detachment was a prerequisite for caspase activation and apoptosis execution. This process therefore resembled "anoikis," a special mode of apoptosis induction in which adherent cells lose contact with the extracellular matrix. Additional experiments with irreversible caspase inhibitors show that MSeA-induced anoikis involved caspase-3- and -7-mediated PARP cleavage that was initiated by caspase-8 and probably amplified through CC-caspase-9 activation and a feedback activation loop from caspase-3. Taken together, the data support a methyl selenium-specific induction of DU-145 cell apoptosis that involves cell detachment as a prerequisite (anoikis) and is executed principally through caspase-8 activation and its cross-talk with multiple caspases.  (+info)

Apoptotic signaling during initiation of detachment-induced apoptosis ("anoikis") of primary human intestinal epithelial cells. (6/360)

Apoptosis after the loss of cell anchorage--"anoikis"--plays an important role in the life cycle of adherent cells. Furthermore, loss of anchorage dependency is believed to be a critical step in metastatic transformation. The aim of this study was to further characterize the sequence of intracellular events during anoikis in a nontransformed population of human intestinal epithelial cells (IECs). Purified human IECs were kept in suspension to induce anoikis in over 90% of IECs within 3 h. Two initiator caspases, caspase-2 and -9, are activated within 15 min, followed by the hierarchical activation of downstream caspases within 1 h. The activation of the caspase FLICE (caspase-8) does not contribute to the initiation of anoikis, and massive release of cytochrome c from mitochondria cannot be detected before 60 min, indicating that cytochrome c release does not play a role during initiation of anoikis. This study delineates the signaling cascade during anoikis of nontransformed cells. Future studies may identify alterations of this cascade in neoplastic cells, thereby possibly gaining insight into carcinogenesis and metastatic transformation.  (+info)

Smad7 inhibits the survival nuclear factor kappaB and potentiates apoptosis in epithelial cells. (7/360)

In this study, we examined the effect of the stable expression of Smad7 in two different cell lines on apoptosis induced by various stimuli including TGF-beta, serum withdrawal, loss of cell adhesion (anoikis) and TNF-alpha. Smad7 increased TGF-beta-mediated apoptosis in Mv1Lu cells as well as anoikis and/or serum withdrawal-induced apoptosis in Mv1Lu and MDCK cells. Smad7 markedly decreased the activity of the survival NF-kappaB transcription factor in MDCK cells. Interestingly, the stable expression of oncogenic Ras in MDCK cells which suppressed Smad7 inhibition of NF-kappaB also suppressed Smad7 potentiation of serum withdrawal-induced apoptosis and anoikis. In addition, Smad7 inhibited TNF-alpha stimulation of NF-kappaB and increased TNF-alpha-mediated apoptosis in MDCK cells. Our results provide the first evidence that Smad7 induces sensitization of cells to different forms of cell death. They moreover demonstrate that Smad7 inhibits the survival NF-kappaB factor, providing a potential mechanism whereby Smad7 potentiates cell death.  (+info)

Human intestinal epithelial cell survival: differentiation state-specific control mechanisms. (8/360)

To investigate whether human intestinal epithelial cell survival involves distinct control mechanisms depending on the state of differentiation, we analyzed the in vitro effects of insulin, pharmacological inhibitors of Fak, MEK/Erk, and PI3-K/Akt, and integrin (beta1, beta4)-blocking antibodies on the survival of the well-established human Caco-2 enterocyte-like and HIEC-6 cryptlike cell models. In addition, relative expression levels of six Bcl-2 homologs (Bcl-2, Bcl-X(L), Mcl-1, Bax, Bak, and Bad) and activation levels of Fak, Erk-2, and Akt were analyzed. Herein, we report that 1) the enterocytic differentiation process results in the establishment of distinct profiles of Bcl-2 homolog expression levels, as well as p125(Fak), p42(Erk-2), and p57(Akt) activated levels; 2) the inhibition of Fak, of the MEK/Erk pathway, or of PI3-K, have distinct impacts on enterocytic cell survival in undifferentiated (subconfluent Caco-2, confluent HIEC-6) and differentiated (30 days postconfluent Caco-2) cells; 3) exposure to insulin and the inhibition of Fak, MEK, and PI3-K resulted in differentiation state-distinct modulations in the expression of each Bcl-2 homolog analyzed; and 4) Fak, beta1 and beta4 integrins, as well as the MEK/Erk and PI3-K/Akt pathways, are distinctively involved in cell survival depending on the state of cell differentiation. Taken together, these data indicate that human intestinal epithelial cell survival is regulated according to differentiation state-specific control mechanisms.  (+info)

Establishment of anoikis-resistant cell model in vitro is usually on the basis of suspension culture that prevents cells from attachment (23-25). Therefore, we chose ultra-low attachment plates for the continuous suspension culture of the parental ACHN cells for 10 days, and the re-adherent cells were regarded as anoikis-resistant ACHN cells. Our data revealed that anoikis-resistant ACHN cells were characterized with more aggressive malignant biological behavior, including more rapid proliferation, less detachment-induced apoptosis and more capable of invasion in contrast to parental cells.. The molecular mechanisms involved in anoikis-resistance have been extensively investigated. PI3Ks are a family of lipid kinases that phosphorylate the 3′-OH group on phosphatidylinositols in the plasma membrane, resulting in recruitment of Akt to cell membrane for activation, which regulates tumor growth and survival (26). Likewise, MEK/ERK is the most typical mitogen activated protein kinase (MAPK) ...
Anoikis resistance is a key to the survival of cells in malignant transformation and metastasis [18, 19]. It may also be a key to the adaptation of cells to suspension culture and spheroids growth used in engineering. For epithelial cells, suppression of anoikis upon detachment seems to be induced when cell-cell contacts are formed. For example, cadherin-mediated homotypic interactions maintain the survival of human prostate carcinoma DU-145 cells in the absence of extracellular matrix (ECM) attachments [20]. Also, disruption of E-cadherin cell-cell contacts showed more important for suppressing anoikis of normal enterocytes after detachment from villus epithelium, as compared to cell-ECM disruption [17]. Growth as spheroids renders tumor cells less sensitive to exogenous apoptotic stimuli, and spheroids have greater drug resistance than the corresponding monolayers [21]; and some cells used in engineering also grow as spheroids in suspension. Thus, elucidating the mechanisms by which spheroids ...
Preclinical and early clinical trials indicate that up to 50% of triple-negative breast cancers (TNBC) express androgen receptor (AR) and are potentially responsive to anti-androgens. However, the function of AR in TNBC and the mechanisms by which AR-targeted therapy reduces tumor burden are largely unknown. We hypothesized that AR maintains a cancer stem cell (CSC)-like tumor initiating population and serves as an anti-apoptotic factor, facilitating anchorage independence and metastasis. AR levels increased in TNBC cells grown in forced suspension culture compared to those in attached conditions, and cells that expressed AR resisted detachment-induced apoptosis. Culturing TNBC cells in suspension increased the CSC-like population, an effect reversed by AR inhibition. Pre-treatment with enzalutamide (Enza) decreased the tumor-initiating capacity of TNBC cells and reduced tumor volume and viability when administered simultaneously or subsequent to the chemotherapeutic paclitaxel; simultaneous ...
Cell culture and chemicals. The human gastric cancer cell lines AGS (CRL-1739; American Type Culture Collection) and MKN28 (JCRB Cell Bank) were grown in monolayer cultures in recommended medium. 2-Methoxyestradiol (2ME2) and diphenyleneiodonium (DPI) chloride were purchased from Sigma-Aldrich and dissolved in DMSO at a concentration of 30 and 10 mmol/L, respectively.. Plasmid construction and production of lentiviral vectors. Short hairpin RNA (shRNA) sequences against human HIF-1α and scrambled control oligonucleotides (TIB MOLBIOL) were published elsewhere ( 3, 4). Oligonucleotides were inserted into BsrGI and XbaI restriction sites of the lentiviral bicistronic vector pPR1, which allows for coexpression of GFP ( 5). Lentiviruses were produced by transient transfection of pPR-HIF-1α or pPR-scr with packaging vectors in 293T cells using the calcium-phosphate method. Vector titers were determined by transducing 293T cells with serial dilutions of concentrated lentivirus, and green fluorescent ...
A form of programmed cell death (apoptosis) induced in certain cell types when they become detached from their extracellular matrix or from a surface. Epithelial, endothelial, and many other tissue cells depend on continual interchange of signals with neighbouring cells and their immediate environment in order to survive. The absence of such signals following detachment from the matrix normally results in death of the cell. However, when tumour cells detach they resist anoikis, allowing them to migrate to new sites and seed new tumours. The reasons for this are unknown: one theory is that overexpression of the NTRK1 receptor for nerve growth factor (see neurotrophin) somehow enables cells to escape anoikis. The term is derived from the Greek word for homelessness. ...
Like soloing rock climbers, adherent cells need a good handhold to survive. Ma et al. now identify an adaptor protein that monitors the cells grip and signals death if the grip fails.. Death following detachment, known as anoikis, is a form of programmed cell death that ensures the disposal of displaced adherent cells. Lack of anoikis is thought to give cells metastatic potential.. A number of survival factors have been identified that are activated by integrin attachment to the extracellular matrix. Binding to soluble matrix fragments, rather than to a fixed matrix, does not prevent anoikis. This difference suggests that mechanical tension is also being measured.. Inside the cell, integrins associate with signaling adaptor proteins of the Shc family. One family member, p66Shc, has been suggested to promote apoptosis. The team now shows that an epithelial cell line that resists anoikis does not express p66Shc. Giving these cells back some p66Shc reestablished detachment-induced death. Normal ...
We identified AKT, p130CAS and focal adhesion kinase (FAK) as novel PTK6 substrates and demonstrated their roles in promoting cell proliferation, migration and resistance to anoikis. In prostate cancer cells, active PTK6 is primarily associated with membrane compartments, although the majority of total PTK6 is localized within the cytoplasm. Ectopic expression of membrane-targeted PTK6 transforms immortalized fibroblasts. Knockdown of endogenous cytoplasmic PTK6 in PC3 prostate cancer cells impairs proliferation, migration and anoikis resistance. However, re-introduction of PTK6 into the nucleus significantly decreases cell proliferation, suggesting context-specific functions for nuclear PTK6. ...
Gender differences are detectable in cardiovascular diseases and reactive oxygen species (ROS) play a pivotal role in the pathogenesis of vascular disease. In this study we aimed to investigate redox state and cell fate in vascular smooth muscle cells (VSMC), which play a role in several cardiovascular diseases, such as hypertension and atherosclerosis, isolated from male and female rat (MVSMC and FVSMC), in basal condition and after induction of oxidative stress by UVB radiation. We found that FVSMC have a more favourable redox balance in comparison with MVSMC both in basal conditions and after UVB irradiation. Accordingly, MVSMC are more susceptible to radiation-induced stress and easier underwent apoptosis in comparison to FVSMC which clearly displayed signs of premature senescence and anoikis resistance that can be due to their cytoskeleton-dependent adhesion features and to a higher propensity to undergo autophagy and survival in unfavourable environmental conditions. Moreover, in FVSMC, ...
Induces apoptosis and anoikis. The isoforms vary in cytotoxicity with isoform BimS being the most potent and isoform BimEL being the least potent.
το κείμενο με τίτλο THREE TOPICS IN PARALLEL COMMUNICATIONS σχετίζετε με Λογισμικό & κατασκευή λογ/κού
Advanced stage cancers acquire anoikis resistance which provides metastatic potential to invade and form tumors at distant sites. Suppression of anoikis resistance by novel molecular therapies would greatly benefit treatment strategies for metastatic cancers. Recently, digitoxin and several of its novel synthetic derivatives, such as -L-rhamnose monosaccharide derivative (D6-MA), have been synthe
Loss of the epithelial adhesion molecule E-cadherin is thought to enable metastasis by disrupting intercellular contacts-an early step in metastatic dissemination. To further investigate the molecular basis of this notion, we use two methods to inhibit E-cadherin function that distinguish between E-cadherins cell-cell adhesion and intracellular signaling functions. Whereas the disruption of cell-cell contacts alone does not enable metastasis, the loss of E-cadherin protein does, through induction of an epithelial-to-mesenchymal transition, invasiveness, and anoikis resistance. We find the E-cadherin binding partner beta-catenin to be necessary, but not sufficient, for induction of these phenotypes. In addition, gene expression analysis shows that E-cadherin loss results in the induction of multiple transcription factors, at least one of which, Twist, is necessary for E-cadherin loss-induced metastasis. These findings indicate that E-cadherin loss in tumors contributes to metastatic ...
Epithelial to mesenchymal transition (EMT) correlates with high-grade malignancy including the competence to form metastases. In addition, EMT has recently been linked to cellular self-renewal programmes of cancer stem cells and apoptosis/anoikis resistance, which are all features of therapeutic resistance. The EMT programme is driven by several transcription factors (TFs), such as the transcriptional regulators SNAIL, SLUG, ZEB1 and ZEB2 and the basic helix-loop-helix factors E47 and TWIST. These proteins target and repress the CDH1 gene, which encodes for E-cadherin, an important caretaker of the epithelial state. Expression studies in human pancreatic cancer showed expression of SNAIL in 78% and of SLUG in 50% of cases.1 Although no or low levels of TWIST are expressed in pancreatic cancers, up-regulation of this gene under hypoxic condition may argue for a contribution towards tumour progression.1 2 Expression of the ZEB2 gene was recently found to be silenced by promoter methylation in the ...
Integrin-mediated adhesion is normally required for cytokinetic abscission, and failure in the process can generate potentially oncogenic tetraploid cells. Here, detachment-induced formation of oncogenic tetraploid cells was analyzed in non-transformed human BJ fibroblasts and BJ expressing SV40LT (BJ-LT) ± overactive HRas. In contrast to BJ and BJ-LT cells, non-adherent BJ-LT-Ras cells recruited ALIX and CHMP4B to the midbody and divided. In detached BJ and BJ-LT cells regression of the cytokinetic furrow was suppressed by intercellular bridge-associated septin; after re-adhesion these cells divided by cytofission, however, some cells became bi-nucleated because of septin reorganization and furrow regression. Adherent bi-nucleated BJ cells became senescent in G1 with p21 accumulation in the nucleus, apparently due to p53 activation since adherent bi-nucleated BJ-LT cells passed through next cell cycle and divided into mono-nucleated tetraploids; the two centrosomes present in bi-nucleated BJ cells
Effects of TCS on anchorage-independent growth of anoikis resistant H460 cells.(A) Cells were pretreated with TCS (0-7.5 µM) for 24 h and subjected to soft a
This study reports on the efficacy and mechanism of action of the small-molecule multikinase inhibitor foretinib in preclinical models of ovarian cancer metastasis. Our data suggest 4 principal mechanisms for how foretinib inhibits ovarian cancer growth and metastasis. In ovarian cancer cell lines, the inhibitor: (i) blocked activation of c-Met signaling; (ii) reduced proliferation mediated by a G2-M cell-cycle arrest; (iii) induced cell death through a 2-step mechanism in which cells detach followed by a caspase-dependent form of anoikis; and (iv) reduced proliferation, adhesion, migration, and invasion during early tumor development. In mouse models of ovarian cancer metastasis, foretinib reduced tumor burden and metastasis mediated by reduced angiogenesis, proliferation, and increased apoptosis. The multiple activities of foretinib are consistent with the numerous effects that have been attributed to c-Met and angiogenesis in the context of cancer (3).. Foretinib targets c-Met and VEGFR-2 ...
Epithelial ovarian cancer is the most lethal gynecological malignancy and the fifth leading cause of cancer death in women in the Western world. ETS transcription factors have been implicated in the regulation of gene expression during a variety of biological processes including cell growth and differentiation. We recently examined the role of the ETS transcription factor ETV5 in epithelial ovarian cancer and described ETV5 as being up-regulated in ovarian tumor samples as compared to ovarian tissue controls. In ovarian cancer cells, we showed that ETV5 regulated the expression of cell adhesion molecules, enhancing ovarian cancer cell survival in anchorage-independent conditions and suggesting that it plays a role in ovarian cancer cell dissemination and metastasis into the peritoneal cavity To understand the role of ETV5 transcription factor during ovarian cancer cell dissemination, we analyzed by gene expression microarray technology those genes whose expression was altered in an ovarian ...
This book focuses on the functional significance of targeting apoptosis for the treatment of prostate cancer. New concepts on the challenges relating to the development of resistance by androgen-independent tumors are introduced, in terms of the contribution of anoikis and cross-talk of androgens with key growth factor signaling pathways. This volume also provides insightful discussion on the exploitation of the apoptotic and angiogenic synergism towards complete eradication of prostate tumors. Last but not least, it includes reflections on the drug development challenge based on the analysis of data from existing clinical trials. ...
Cell detachment upregulates Fas expression in HUVECs. (A) Detachment induces cell surface levels of Fas. HUVECs were kept adherent or in suspension for 12 h. FA
A drill bit offering improved steerability. Drill bits include gage sections which are adapted to facilitate deflection of the bits within a borehole to facilitate navigational or directional drilling. The gage portions of the bit may be arranged in an arcuate path around a portion of the periphery of the bit. Also, the bit portions may be spaced and adapted to serve, at least in part, as fulcrums, to facilitate deflection of the bit and the bringing of gage cutting portions of the bit in contact with the sidewalls of the borehole.
NOTE 1 - When a 6-bit spare is needed to satisfy the 8-bit byte boundary rule, the 6-bit spare will be interpreted as a valid 6-bit character (all zeros is the "@" character). This is the case when the number of characters is: 1, 5, 9, 13,17, 21, 25, etc ...
Posted a comment on discussion Open Discussion on Practically Random Well, youve got correct numbers, now. Question: Why are you calling them 63-bit numbers? If they have sign, then they can still be ordered as 64-bit numbers. So, treat them as 64-bit numbers and call it good. For this test it does not actually matter whether you order them as signed or unsigned. Hopefully. They are 63 bit values because they are made by taking the most significant 21 bits from 3 consecutive 32-bit PRNG outputs and concatonating them. 21 times 3 is 63. The 63 bits are stored in 64... ...
Tumor cells that acquire metastatic potential have developed resistance to anoikis, a cell death process, after detachment from their primary site to the second organ. In this study, we investigated the molecular mechanisms of a novel marine bacterial polysaccharide EPS11 which exerts its cytotoxic effects through affecting cancer cell adhesion and anoikis. Firstly, we found that EPS11 could significantly affect cell proliferation and block cell adhesion in A549 cells. We further demonstrated that the expression of several cell adhesion associated proteins is downregulated and the filiform structures of cancer cells are destroyed after EPS11 treatment. Interestingly, the destruction of filiform structures in A549 cells by EPS11 is in a dose-dependent manner, and the inhibitory tendency is very consistent with that observed in the cell adhesion assay, which confirms that filiform structures play important roles in modulating cell adhesion. Moreover, we showed that EPS11 induces apoptosis of A549 ...
E-cadherin is synthesized as a precursor and then undergoes cleavage by proprotein convertases. This processing is essential for E-cadherin maturation and cell adhesion. Loss of cell adhesion causes detachment-induced apoptosis- anoikis. Anoikis can be inhibited despite loss of cell-matrix interactions by preserving E-cadherin mediated cell-cell adhesion. Conversely, acute loss of E-cadherin sensitizes cells to apoptosis by unknown post-translational mechanisms. In response to drug treatment of breast cancer cells, our analysis revealed that two independent modifications of E-cadherin inhibit its cell surface transport. Firstly, O-linked beta-N-acetylglucosamine (O-GlcNAc) modification of the cytoplasmic domain retains E-cadherin in the endoplasmic reticulum. Secondly, incomplete processing by proprotein convertases arrests E-cadherin transport late in the secretory pathway. We demonstrated these E-cadherin modifications (detected by specific lectins and antibodies) do not affect binding to ...
In endometriosis, the increased survival potential of shed endometrial cells (which normally undergo anoikis) is suggested to promote lesion development. One mechanism that may alter anoikis is autophagy. Using an autophagic flux inhibitor hydroxychloroquine (HCQ), we identified that it reduces the in vitro survival capacity of human endometriotic and endometrial T-HESC cells. We also identified that HCQ could decrease lesion numbers and disrupt lesion histopathology, as well as increase the levels of peritoneal macrophages and the IP-10 (10 kDa interferon-γ-induced protein) chemokine in a mouse model of endometriosis. We noted that RNA levels of a subset of autophagic markers were reduced in lesions relative to uterine horns from endometriosis-induced (untreated) mice. In addition, the RNA levels of autophagic markers were decreased in uterine horns of endometriosis-induced mice compared with those from controls. However, we noted that protein expression of LC3B (microtubule-associated protein ...
The University of Auckland Library Trefoil Factor-1 (TFF1) belongs to the family of trefoil factor peptides. Trefoil factors protect the gastrointestinal tract against mucosal injury. Trefoil peptides are upregulated and secreted in an autocrine and paracrine fashion in response to gastrointestinal injury. They facilitate cell migration and prevent anoikis. TFF1 is also expressed in various tissues and regulated by multiple cellular processes. Several studies have also demonstrated increased expression of TFF1 in a high percentage of mammary and prostate carcinoma cases. However, the functional role of autocrine TFF1 in mammary and prostate carcinoma has not been previously elucidated. Herein, I demonstrate that forced expression of TFF1 in mammary carcinoma cells resulted in increased total cell number as a consequence of increased cell proliferation and survival. Forced expression of TFF1 enhanced anchorage-independent growth and promoted scattered cell morphology with increased cell migration ...
Cancer is a dominant and common disease that claims the lives of many people in the world. Metastasis is a type of cancer that is characterized by malignancy. Metastasis is the combination of the early invasion and late colonization of cancer cells. Learn more about Oncotarget at Research Gate. Typically, cancer cells experience morphological transformation and change their cell-cell matrix connection to pass through the first stage of the multistep process of metastasis. The epithelial-mesenchymal transition (EMT) is a critical stage in the early events of tumor cell metastatic supply by supporting the cells with more invasive, motile potential. On the other side, Mesenchymal-epithelial transition (MET) is needed to move the cells to extravasated from the vessels into their tissue to create micrometastases. The micrometastases will eventually develop a secondary tumor after the cells survive anoikis process. Check Oncotarget journal at scimagojr.com. Long-coding RNAs (LncRNAs) are categories of ...
Intraperitoneal "seeding" is a distinctive pattern of dissemination that is unique to EOC and markedly differs from the hematogenous or lymphatic metastasis found for many other types of tumors. A key and initial rate-limiting step in the "seeding" of EOC is the survival of floating tumor cells in the peritoneal fluid. It is widely recognized that aggregation enables floating tumor cells to escape anoikis, although it is unclear whether tumor cells shed into the peritoneal fluid as aggregates or shed as single cells that then assemble into aggregates (3). The mechanisms that mediate adhesion between floating EOC cells are poorly understood. EOC cells express several integrins and extracellular matrix (ECM) proteins, and interactions between α5β1 integrin and fibronectin have been reported to mediate assembly of EOC cells into spheroids (22). Cadherins are transmembrane glycoproteins that have well-established functions in mediating homophilic cell adhesion (7). The role of cadherins in ...
A transmission apparatus and method turbo-encode data and output systematic bit and parity bit data. The systematic bit data and the parity bit data are modulated independently of each other such that communication quality is better when a modulation scheme for the systematic bit data is changed than when a modulation scheme for the parity bit data is changed. The systematic bit data and the parity bit data are then transmitted.
Definition of parity bit in US English - a bit which acts as a check on a set of binary values, calculated in such a way that the number of 1s in the set plus th
Little bit of blood in discharge - Little bit if bright red blood & white creamy discharge, what is this? Period. Could be the beginning of your period or poss. Mis.
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Bitfields for Digiboard initializing parameters: Bit(s) Description ) 7-5 unused 4-3 parity (00 none, 01 odd, 11 even) 2 stop bits (0 = one, 1 = two) 1-0 data bits (00 = five, 01 = six, 10 = seven, 11 = eight) SeeAlso: #00307,#00308 ...
and sex is a bit painful (esp upon entry) Sometimes I even bleed a small bit. I am sore for a few days afterwards. Anyone else have this problem?? Just started happening to me. ...
TY - JOUR. T1 - Extracellular matrix metalloproteinase inducer (CD147) confers resistance of breast cancer cells to anoikis through inhibition of bim. AU - Yang, Jin Ming. AU - ONeill, Peter. AU - Jin, Wei. AU - Foty, Ramsey. AU - Medina, Daniel J.. AU - Xu, Zude. AU - Lomas, Mehnaaz. AU - Arndt, Greg M.. AU - Tang, Yi. AU - Nakada, Marian. AU - Yan, Li. AU - Hait, William N.. PY - 2006/4/7. Y1 - 2006/4/7. N2 - Overexpression of extracellular matrix metalloproteinase inducer (EMMPRIN or CD147), a member of the immunoglobulin family and a glycoprotein enriched on the surface of tumor cells, promotes invasion, metastasis, and growth and survival of malignant cells and confers resistance to some chemotherapeutic drugs. However, the molecular mechanisms underlying the actions of EMMPRIN are not fully understood. In this study we sought to determine whether EMMPRIN contributes to the malignant phenotype of breast cancer by inhibiting anoikis, a form of apoptosis induced by loss or alteration of ...
elements no longer contain values stretching over multiple 64-bit fields. If number of bits per block is not power of two (i.e. single 64-bit value cant fill whole number of blockstates) some bits will not be used. For example, if single block state takes 5 bits, highest 4 bits of every 64-bit field will be unused. That also means slight increase in storage size (in case of 5 bits, from 320 to 342 64-bit fields).. ...
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I am trying to run defrag but it tells me that the NTFS Dirty Bit is set. So I scheduled chechdisk to run at next boot (but it fails). How can I reset the NTFS Dirty Bit without using chkdisk or...
When I watched the TED talk on Little Bits, I knew I was going to have to get a set for my son. Little Bits are intended for children 8 to ∞.
Am I happy with it? Mostly, I am not happy with the way the checks sit in the shunting yard, all a bit wonky. But I am not going to un-stitch .. I have un-stitched enough ...
Hello, Ive installed the newest version of slackware, and Im not very good at working the system. I have two questions... My screen size is set at 6
MP1026B 眼圖分析儀, 掌上型、堅固耐用的解決方案,能夠對數據傳輸率為0.1到12.5Gbps的數據執行眼圖量測
The integrin family of cell surface receptors is evolutionary conserved and found in all multicellular animals. In humans 8-alpha and 18-beta integrins are non-covalently associated into 24 dimers. Integrins mediate cell-extracellular matrix and cell-cell interactions and participate in cell signalling. This ideally places integrins to regulate vital processes such as cell adhesion, migration, differentiation and cytoskeleton dynamics. Integrins also play a fundamental role in regulating cell survival and anoikis. In this thesis molecular mechanisms employed by integrins to induce signal transduction, independently or through crosstalk with other receptors, were characterised.. Rictor-mTOR (mTORC2) was required for Akt Ser473 phosphorylation in response to β1 integrin-mediated adhesion as well as EGF-, PDGF- or LPA-stimulation of MCF7 cells. ILK and PAK were dispensable for Akt Ser473 phosphorylation upon β1 integrin-engagement or EGF-stimulation. PAK was needed when this phosphorylation was ...
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A parity bit, or check bit, is a bit added to a string of binary code to ensure that the total number of 1-bits in the string is even or odd.[1] Parity bits are used as the simplest form of error detecting code. There are two variants of parity bits: even parity bit and odd parity bit. In the case of even parity, for a given set of bits, the occurrences of bits whose value is 1 is counted. If that count is odd, the parity bit value is set to 1, making the total count of occurrences of 1s in the whole set (including the parity bit) an even number. If the count of 1s in a given set of bits is already even, the parity bits value is 0. In the case of odd parity, the coding is reversed. For a given set of bits, if the count of bits with a value of 1 is even, the parity bit value is set to 1 making the total count of 1s in the whole set (including the parity bit) an odd number. If the count of bits with a value of 1 is odd, the count is already odd so the parity bits value is 0. Even parity is a ...
No, a 64bit executable is a 64bit executable is a 64bit executable. The two separate directories exist to make it easier to maintain a 32 bit and 64 bit copy of an application, as far as I can tell.. You will need to recompile your things for 64bit, as the location of an executable makes no difference to how it is executed.. ...
What is UART UART Communication Protocol How does UART Protocol Work UART Protocol Data Sending and Receiving (Tx - Rx) Start Bit Main Data Parity Bit End Bit Calculate the Desired Speed and Time Required for Communication in the UART Protocol UART Protocol Result UART Protocol MikroC Library Functions UART_VERI_TAMPONU General Series UART_ESLIK_BIT_HESAPLAMA Function UART_GONDERILECEK_VERI_AYIKLAMA Function UART_VERI_GONDER Function […]. ...
I may need to upgrade to Excel 64-bit in order to handle increasingly larger backtest/analysis files (|150MB) that seem to cause 32-bit to constantly...
Thats a bit harsh. I mean...ass wad ? Whos the ass now? No ones the ass now. You are the donkeys gonads, thats all ...
A little bit of gameplay - video shows an underleveled Ranger going full man-mode on a Hellspawn. You can see new interface in action, as well as spells for...
I ADORE Tiffany. Maybe a bit too much. In fact, if you knew who Tiffany was, youd like her too. Lately, Ive been on a spring cleaning rampage and Tiffany did me GOOD! She helped me get totally organized. But thats not all, she got things organized and made them pretty. For me, thats a…
LPA stimulates growth, prevents apoptosis and anoikis, decreases sensitivity to chemotherapeutic drugs, increases production of neovascularization mediators, and increases invasiveness of ovarian cancer cells (12) . LPA levels are elevated in ascites and plasma from ovarian cancer patients, implicating it in ovarian tumorigenesis (2, 3, 4, 5, 6) . Because LPA levels are higher in ascitic fluid than in plasma, it has been hypothesized that LPA is produced in the peritoneal cavity and then migrates to the peripheral circulation. Ovarian cancer cells have been implicated to be the source of LPA production in ascites, because they have been shown to synthesize LPA in response to the tumor-promoting agent PMA (28) . However, whether PMA mimics a physiological process is not known. Ovarian cancer cells in the patient might produce LPA either constitutively or after activation by the cellular milieu. Knowledge of regulation of LPA production by ovarian cancer cells and the enzymes involved in LPA ...
What kind of message(s) forces a cell to reprogram itself for the flight reaction? Recent years have brought about some intriguing discoveries. On the one hand, cells that have sustained and accumulated a critical level of DNA damage are destined to collapse their focal contacts with the surrounding matrix proteins and undergo apoptotic death (reviewed in Ref. 92). Stress-induced changes in cell-matrix adhesion initiate the flight reaction, which may, eventually, result in anoikis (22, 56). Here, cell adhesion to its matrix serves as a sensor of the severity of stress, triggering cell exfoliation and suicide. Both reactions appear to be "altruistic" in the sense that they protect the organism from the accumulation of genetically compromised cells.. Stress-induced changes in cell-matrix adhesion occur via several routes that invariably lead to the disassembly of the focal adhesion complexes (matrix protein-integrin receptor-recruited adaptor proteins of the focal adhesion-cytoskeleton axis). The ...
3-D matrices such as collagen gel have previously been shown to promote survival and differentiation of islets in culture (14-19), but neither their effect on proliferation nor the mechanisms responsible for their beneficial effect have been studied. In this report, we show that a 3-D fibrin matrix support improves survival, reduces apoptosis, and allows for HGF-mediated proliferation of islet cells, leading to increased β-cell mass without loss of function.. Previous data have shown that islet proliferation needs the interaction in monolayer with matrices such as 804G or HTB-9 (2,3). Our findings in this report show that although growth factors are ineffective in islets that are free floating, cellular interaction in a 3-D configuration with a fibrin matrix allows proliferation to occur. Thus, avoiding cell growth in monolayer eliminates the need to disrupt cell matrix interactions and subsequent anoikis (7). Moreover, we show that glucose-responsive β-cell function is not impaired in ...
0221] In the auxiliary mode, each bit to be decoded of the first Xf and second X1 codeword bit sequence is calculated or determined based on i) a bit of a predefined bit position within the first Xf or second X1 codeword bit sequence, preferably within the second codeword bit sequence X1, and ii) another bit of the first Xf or second X1 codeword bit sequence at a bit position defined based on the bit to be decoded. This is in clear contrast to the default mode, where each bit to be decoded of the first Xf and second X1 codeword bit sequence is calculated or determined solely on a bit of the first Xf or second X1 codeword bit sequence at a bit position defined based on the bit to be decoded. As a consequence, if the two codeword bit sequences Xf, X1 each comprises N bits, 2N bits of the two bit sequences Xf, X1 will carry payload information for encoding the original properties or features of the image element in the default mode. However, in the auxiliary mode only 2N-1 bits of the codeword bit ...
|p|This Bahco 31 piece bit set comprises the following;|/p||p|5 x 1/4 inch Pozidriv bits: PZ1, PZ2 (x3) and PZ3. |br|5 x 1/4 inch Phillips bits: PH1, PH2 (x3) and PH3. |br|2 x 1/4 inch Slim Phillips bits: PH2G (x2). |br|11 x 1/4 inch Torx bits: T10, T15 (
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When Windows thinks your hard disk or USB flash drive needs scanning for errors, it will enable a hidden setting on the drive and will keep asking to scan until you allow it. Heres how to manually clear the dirty bit without running a ChkDsk. - Page 2
so it should be illegal? Seems a fair bit tamer than the destruction alcohol or other hard drugs can wreck.... YOU HAVE RUINED MY LIFE BECAUSE YOU GET AGG - #90510644 added by happyfox at all natural
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With regard to TIMP 3, the total amount of this protein associated with the matrices of confluent stromal cell cultures of normal corneas maintained over a period of time of 8e10 days was approximately 5-fold higher than that within their regularly obtained culture media examples. After infecting stromal cells with RAdTIMP 3 very little of the freshly synthesised TIMP 3 was recovered in their culture media but the quantity connected with the matrices, which was measured 13 days after infection, was significantly more than normally present. Normal corneal stromal cell cultures, when 70-80 Cabozantinib price confluent infected with RAdTIMP 3, all showed symptoms of cell death between day 2 and 5 after infection. As well as the appearance of detached cells in the growth medium, significant pockets developed. As shown in Fig. 3a, these were without both cells and matrix and, because of the unusually dense packing of cells round the holes, appeared to be due to matrix contraction. Eventually ...
I am resurrecting this old thread since this is at the top of search results for 32-bit Access drivers on 64-bit Windows 7 and because the accepted answer is completely wrong.. The 32-bit ODBC is in the SysWow64 directory and the 64-bit ODBC is in the System32 directory. If you have 32-bit Office installed or if you have no Office installed, you can use the Office 2010 Redistributable files that others have linked. If you have 64-bit Office installed, the 32-bit redistributable files will NOT install. Instead it wants to force you to uninstall 64-bit Office first. This is pretty severe for just a 32-bit driver! (yes I understand there is more to this than the driver.. My point still stands - it is pretty severe).. To get around this problem, you must install the 32-bit redistributable files from the command line and pass the argument /passive to it:. C:\MyDir\, AccessDatabaseEngine.exe /passive. By using this option I have successfully installed the 32-bit drivers on my 64-bit system and am able ...
I am resurrecting this old thread since this is at the top of search results for 32-bit Access drivers on 64-bit Windows 7 and because the accepted answer is completely wrong.. The 32-bit ODBC is in the SysWow64 directory and the 64-bit ODBC is in the System32 directory. If you have 32-bit Office installed or if you have no Office installed, you can use the Office 2010 Redistributable files that others have linked. If you have 64-bit Office installed, the 32-bit redistributable files will NOT install. Instead it wants to force you to uninstall 64-bit Office first. This is pretty severe for just a 32-bit driver! (yes I understand there is more to this than the driver.. My point still stands - it is pretty severe).. To get around this problem, you must install the 32-bit redistributable files from the command line and pass the argument /passive to it:. C:\MyDir\, AccessDatabaseEngine.exe /passive. By using this option I have successfully installed the 32-bit drivers on my 64-bit system and am able ...
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Today Dwight Silverman ran a great piece on TechBlog which examines whether folks buying a new PC are best sticking with 32-bit Vista or making the leap to 64-bit Vista. Its a good piece but theres one bit that I feel deserves some clarification.
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Years later, we finally got ourselves our own Waffle machine (a little bit like this one - we have a sunbeam, but they dont make them anymore) and we tend to drag it out on a sunday morning ... German Waffles are not as deep as the Belgium Waffles, they tend to be thin, more like pancakes ...
Clusterin, ubiquitously distributed in mammalians, was cloned and identified as the most potently induced gene during rat prostate involution following androgen deprivation. Also found to be involved in many other patho-physiological processes, its biological significance is still controversial, particularly with regard to apoptosis. We previously showed that transient over-expression of clusterin blocked cell cycle progression of simian-virus-40-immortalized human prostate epithelial cell lines PNT1A and PNT2. We show in the present study that the accumulation of an intracellular 45 kDa clusterin isoform was an early event closely associated with death of PNT1A cells caused by cell detachment followed by apoptosis induction (anoikis). Cell morphological changes, decreased proliferation rate and cell cycle arrest at G0/G1-S-phase checkpoint were all strictly associated with the production and early translocation to the nucleus of a 45 kDa clusterin isoform. Later, nuclear clusterin was found ...
Signals from the extracellular matrix are essential for the survival of many cell types. the classically observed survival-promoting one by the intensity of the kinase activation. The disappearance of the GTP-bound forms of Rac1 and Cdc42 gives rise to proapoptotic moderate activation of the Raf-MEK-Erk cascade via a signaling pathway involving the kinases phosphatidlyinositol 3-kinase and Akt. Moreover concomitant activation of p53 and inhibition of SB 203580 Akt are both necessary and sufficient to signal anoikis in primary fibroblasts. Our data demonstrate that the GTPases of the Rho family control three major components of cellular signal transduction namely p53 Akt and Erks which collaborate in the induction of apoptosis due to the loss of anchorage. Rabbit polyclonal to Caspase 9.This gene encodes a protein which is a member of the cysteine-aspartic acid protease (caspase) family.. Elimination by apoptosis is a frequent cellular destiny: essential in normal physiology its deregulation is ...
If you have a .Net application that has been compiled with the target CPU option set to AnyCPU (as opposed to x86 / 32bit or x64 / 64bit specifically) and you are running a 64bit operating system, that application will automatically run as a 64bit process. If you run it on a 32bit machine, it will run in a 32bit mode.. You can however change the CorFlags of the executable, to force it to run as a 32bit process, even if you are running a 64bit operating system. This process changes the headers of the .Net portable executable file.. The CorFlags.exe tool that gets installed with Visual Studio can be used to change the CorFlags.. Change the CorFlags. Open a "Visual Studio Command Prompt" or "Developer Command Prompt" depending on your version of Visual Studio ...
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Thankyou. I write a bit of this, a bit of that. Im currently writing a 30s Noir Thriller/Mystery, its coming along slowly, but well. Nice to see a fellow wri - #99487205 added by wilvine at Women
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So i have been noticing for a while that sometimes when mimi walks she doesnt always bend her back legs, she does when she is running and jumping and when we go out for walks but today i was just watching her playing with her toys and i notice she has a little bit of a wobble at the back knee area, i ran to tell my mom to see if i was just imagining it but then mimi realised she was getting more attention so just sat down and waited for a treat lol, but i am a little bit worried now about
So I am using cryptopp to encrypt a file in a project and I am using AES-GCM. I have a 256bit key and a 128bit ivec and a 128bit tag that I use to encrypt files. However, I want to know where the ...
Being right all the time doesnt help me in my quest to be a bit more modest. It does, however, help me spend a bit more time with those whom I care about. Having drunk so much of it in London, Im amazed at my ability to be thrilled by cats piss.
Hiya! Need a bit of help, has anyone else had changes to there totm. I have never been regular as I have pcos but since starting 17:05:51 I am...
Anoikis; and, in BLT2-overexpressing PWR-1E non-malignant prostate cells, 12(S)-HETE diminish anoikis-induced apoptosis. ith ... cascade following detachment confers anoikis resistance in prostate cancer cells". Journal of Biological Chemistry. 288 (42): ...
Zvibel I, Smets F, Soriano H (2002). "Anoikis: roadblock to cell transplantation?". Cell Transplantation. Cognizant ... single-cell suspensions subject surviving cells to harsh chemical or mechanical forces that may sensitize cells to anoikis, ...
Zvibel I, Smets F, Soriano H (2002). "Anoikis: roadblock to cell transplantation?". Cell Transplantation. 11 (7): 621-30. doi: ... single-cell suspensions subject surviving cells to harsh chemical or mechanical forces that may sensitize cells to anoikis, ...
... in anoikis". J. Biol. Chem. 279 (43): 44667-72. doi:10.1074/jbc.M408101200. PMID 15302871. Sasaki H, Ide N, Yukiue H, Kobayashi ... in anoikis". The Journal of Biological Chemistry. 279 (43): 44667-72. doi:10.1074/jbc.M408101200. PMID 15302871. Han MJ, Chiu ... resulting in a type of extracellular apoptosis called anoikis. Moreover, DAP3 may contribute to apoptosis through its mediation ...
... contributes to tumor growth and protects cells from anoikis, a form of programmed cell death induced when contact- ... Terada LS, Nwariaku FE (2011). "Escaping Anoikis through ROS: ANGPTL4 controls integrin signaling through Nox1". Cancer Cell. ... H2O2 ratio and confers anoikis resistance to tumors". Cancer Cell. 19 (3): 401-415. doi:10.1016/j.ccr.2011.01.018. PMID ...
2002). "Hp95 promotes anoikis and inhibits tumorigenicity of HeLa cells". Oncogene. 21 (44): 6801-8. doi:10.1038/sj.onc.1205849 ...
Yamaki N, Negishi M, Katoh H (August 2007). "RhoG regulates anoikis through a phosphatidylinositol 3-kinase-dependent mechanism ... protection from anoikis and regulation of the neutrophil NADPH oxidase. As with all small G proteins RhoG is able to signal to ...
... or anoikis. Though it has not been observed to localize to the cell membrane, it can be found in the outer cell surface. Its ... "Eukaryotic translation elongation factor 1A induces anoikis by triggering cell detachment". The Journal of Biological Chemistry ...
Approximately 2,500 of these systems are known as Anoikis or 'Wormhole Space.' Systems in Anoikis lack stargates or other ...
"Hepatitis B virus X protein confers resistance of hepatoma cells to anoikis by up-regulating and activating p21-activated ... "Klotho endows hepatoma cells with resistance to anoikis via VEGFR2/PAK1 activation in hepatocellular carcinoma". PLoS One. 8 (3 ... "N-acetylglucosaminyltransferase V confers hepatoma cells with resistance to anoikis through EGFR/PAK1 activation". Glycobiology ...
Frisch SM (2000). "Evidence for a function of death-receptor-related, death-domain-containing proteins in anoikis". Curr. Biol ...
November 23, 2012). "CCN2 inhibits lung cancer metastasis through promoting DAPK-dependent anoikis and inducing EGFR ...
Anoikis Apaf-1 Apo2.7 Apoptotic DNA fragmentation Atromentin induces apoptosis in human leukemia U937 cells. Autolysis ...
"CUB domain-containing protein 1 is a novel regulator of anoikis resistance in lung adenocarcinoma". Molecular and Cellular ...
Cleavage can cause cell death by anoikis and release alarmins from the ECM inducing inflammation. Fragments of fibronectin can ...
"ERK-regulated αB-crystallin induction by matrix detachment inhibits anoikis and promotes lung metastasis in vivo". Oncogene. 34 ...
Other forms of programmed cell death include anoikis, almost identical to apoptosis except in its induction; cornification, a ... Anoikis Apoptosis-inducing factor Apoptosis versus Pseudoapoptosis Apoptosome Apoptotic DNA fragmentation Autolysis (biology) ...
Other forms of programmed cell death include anoikis, almost identical to apoptosis except in its induction; cornification, a ...
2004). "CEACAM6 gene silencing impairs anoikis resistance and in vivo metastatic ability of pancreatic adenocarcinoma cells". ...
... sensitized MDA-MB231 and HBC4 to anoikis, i.e., upon treatment with U0126, cells deprived of anchorage entered apoptosis ... Loss of contact with substratum triggers apoptosis in many normal cell types, a phenomenon termed anoikis. ... inhibitors restore anoikis sensitivity in human breast cancer cell lines with a constitutively activated extracellular- ...
Matarrese P, Conti L, Varano B, Gauzzi MC, Belardelli F, Gessani S, Malorni W (2000). "The HIV-1 vpr protein induces anoikis- ...
2000). "The HIV-1 vpr protein induces anoikis-resistance by modulating cell adhesion process and microfilament system assembly ...
2007). "Functional role and oncogene-regulated expression of the BH3-only factor Bmf in mammary epithelial anoikis and ... activated by anoikis". Science. 293 (5536): 1829-32. doi:10.1126/science.1062257. PMID 11546872. "Entrez Gene: BMF Bcl2 ...
... activated by anoikis". Science. 293 (5536): 1829-32. doi:10.1126/science.1062257. PMID 11546872. Fuhrmann JC, Kins S, Rostaing ... activated by anoikis". Science. United States. 293 (5536): 1829-32. doi:10.1126/science.1062257. ISSN 0036-8075. PMID 11546872 ...
... activated by anoikis". Science. 293 (5536): 1829-32. Bibcode:2001Sci...293.1829P. doi:10.1126/science.1062257. PMID 11546872. ...
Silenced expression of GPR56 in HeLa cells enhanced apoptosis and anoikis, but suppressed anchorage-independent growth and cell ...
Anoikis is a specific type of apoptosis induced by loss of cell adhesion or inappropriate cell adhesion (8). Anoikis plays a ... Anoikis is a specific type of apoptosis that plays a vital physiological role in regulating tissue homoeostasis. Anoikis- ... Anoikis-resistance inhibits detachment-induced apoptosis, promoting proliferation and invasion in ACHN cells. Anoikis-resistant ... TrkB silencing enhances anticancer efficiency of sorafenib in anoikis-resistant ACHN cells. (A) Anoikis-resistant ACHN cells (5 ...
Because anoikis deficiency is a key feature of neoplastic transformation and invasive growth of epithelial cancer cells, our ... Because anoikis deficiency is a key feature of neoplastic transformation and invasive growth of epithelial cancer cells, our ... Because anoikis deficiency is a key feature of neoplastic transformation and invasive growth of epithelial cancer cells, our ... Because anoikis deficiency is a key feature of neoplastic transformation and invasive growth of epithelial cancer cells, our ...
Anoikis mechanisms.. Frisch SM1, Screaton RA.. Author information. 1. The Burnham Institute, 10901 North Torrey Pines Road, La ... Anoikis is defined as apoptosis that is induced by inadequate or inappropriate cell-matrix interactions. It is involved in a ... The central problem of anoikis is to understand how integrin-mediated cell adhesion signals control the apoptotic machinery. In ... particular, the initiation of the caspase cascade in anoikis remains to be explained. ...
The word Anoikis was coined by Frisch and Francis in a paper published in the Journal of Cell Biology in 1994. Anoikis, in ... Given that FLIP is an inhibitor of anoikis, and that reducing FLIP can sensitize metastatic cells to anoikis, Mawji et al. ... Anoikis is a form of programmed cell death that occurs in anchorage-dependent cells when they detach from the surrounding ... When cells are detached from the ECM, there is a loss of normal cell-matrix interactions, and they may undergo anoikis. However ...
Normal cells undergo anoikis when they lose adhesion to or encounter an inappropriate extracellular matrix. By contrast, ... Depletion of Bim together with Bad has an additive effect on protecting B-RAF knockdown cells from anoikis. Together, our data ... Mutant B-RAF mediates resistance to anoikis via Bad and Bim.. Boisvert-Adamo K1, Aplin AE. ... Increased Bim(EL) levels induce apoptosis in suspended cells and are required for anoikis in B-RAF-depleted cells. ...
Retrieved from "http://www.ganfyd.org/index.php?title=Anoikis". Categories: Medical etymology , Medical Dictionary , Basic ...
These results establish HO-1 as a mediator of ATF4-dependent anoikis resistance and tumor metastasis and suggest ATF4 and HO-1 ... ATF4-dependent induction of heme oxygenase 1 prevents anoikis and promotes metastasis. ... ATF4-dependent induction of heme oxygenase 1 prevents anoikis and promotes metastasis. ... and reconstitution of ATF4 or HO-1 expression in ATF4-deficient cells blocked anoikis and rescued tumor lung colonization. HO-1 ...
... anoikis). As the negative pressure is thought to play a role in the anoikis process, these results have implications for both ... a form of cell death known as anoikis. In this study, we set levels of pressure(negative and positive pressure) loaded ECs ... anoikis). As the negative pressure is thought to play a role in the anoikis process, these results have implications for both ... Hu, J. , Zhang, E. , Wu, J. , Xu, W. , Chen, H. , Shi, Y. and Guo, Y. (2010) Pressure shift mediated anoikis of endothelial ...
American Journal of Physiology - Cell Physiology® and the APS® logo are registered trademarks of the American Physiological Society , Print ISSN: 0363-6143 , Online ISSN: 1522-1563. ...
Suppression of anoikis resistance by novel molecular therapies would greatly benefit treatment strategies for metastatic ... Advanced stage cancers acquire anoikis resistance which provides metastatic potential to invade and form tumors at distant ... In addition, D6-MA also targeted Mcl-1 degradation causing an increased anoikis in A549 lung cancer cells. Anoikis sensitizing ... Suppression of anoikis resistance by novel molecular therapies would greatly benefit treatment strategies for metastatic ...
... efficiently triggered anoikis of ras-transformed cells. Thus, oncogenic ras can prevent Chk2 from triggering anoikis even when ... a known inhibitor of anoikis, remain anoikis-resistant in response to enforced Chk2 upregulation. By contrast, drugs, such as ... Tumor suppressor protein kinase Chk2 is a mediator of anoikis of intestinal epithelial cells.. [Byong Hoon Yoo, Alexander ... We conclude that Chk-2 is an important novel component of anoikis-promoting machinery of intestinal epithelial cells. ...
CCN2 inhibits lung cancer metastasis through promoting DAPK-dependent anoikis and inducing EGFR degradation.. [C-C Chang, M-H ... In this study, we investigate the role of CCN2 in anoikis, a form of programmed cell death that is critical in suppressing ... which leads to anoikis. Overall, our findings provide evidence validating the use of CCN2 as an anti-metastatic therapy in lung ...
Abstract 2856: Inhibition of glycolysis sensitizes cancer cells to metformin-induced anoikis. Yong Yi and Zhi-Xiong Jim Xiao ... Inhibition of glycolysis sensitizes cancer cells to metformin-induced anoikis. [abstract]. In: Proceedings of the 107th Annual ... Abstract 2852: CITED2, an emerging regulator in hypoxia- and anoikis- mediated cancer cell growth ... Abstract 2856: Inhibition of glycolysis sensitizes cancer cells to metformin-induced anoikis ...
A 4- to 5-fold increase of anoikis was detected in AGS KD cells compared with control cells. B, anoikis of AGS KD and SCR cells ... Effects of HIF-1α inhibition on anoikis. For induction of anoikis, AGS cells were cultivated on polyHEMA-coated dishes and ... Both variables revealed a significant induction of anoikis in 2ME2-treated cells, confirming enhanced susceptibility to anoikis ... effect of DPI on anoikis. AGS KD cells were treated for 24 h with 5 μmol/L DPI, and anoikis was quantitated by activation of ...
Moreover, we showed that EPS11 induces apoptosis of A549 cells through stimulating βIII-tubulin associated anoikis: (i) EPS11 ... Tumor cells that acquire metastatic potential have developed resistance to anoikis, a cell death process, after detachment from ... marine bacterial polysaccharide EPS11 which exerts its cytotoxic effects through affecting cancer cell adhesion and anoikis. ... cell lung carcinoma treatment via blocking filiform structure mediated adhesion and stimulating βIII-tubulin associated anoikis ...
PD98059 Renders MDA-MB231 Cells Anoikis Sensitive, But Induction of Anoikis Sensitivity in HBC4 Cells Requires Further Addition ... Induction of Anoikis Sensitivity in MDA-MB231 and HBC4 Cells Requires Concurrent Inhibition of ERK and p70S6K Pathways.. The ... This phenomenon resembles anoikis, a form of apoptosis that occurs in various cell types upon detachment from the extracellular ... Anoikis is an important physiological mechanism to prevent ectopic survival of displaced cells, and its strict control is ...
GSE causes anoikis and decreases FAK levels in LNCaP cells. A, cells were treated with GSE (20 μg/mL) for 12 h and cell ... GSE Causes Anoikis in LNCaP Cells and Decreases FAK Levels. During the entire cell growth and viability assay, we also examined ... GSE-induced anoikis and apoptosis were accompanied by a strong decrease in focal adhesion kinase levels, but an increase in ... Based on the results showing that GSE causes a strong death of LNCaP cells together with its anoikis effect, next studies were ...
Anoikis assay and colony formation assay. Anoikis resistance was determined and quantified as described previously (Derksen et ... Wnt11 regulates RhoA-dependent anoikis resistance in mILC. (A) Knockdown of Wnt11 in mILC-1 Wnt11-iKD cells reduces anoikis ... D) Rho controls anoikis resistance of mILC cells. Inhibition of Rho by cell-permeable C3 transferase leads to inhibition of ... Using anoikis-resistant mILC cell lines we now identify (candidate) Kaiso target genes including Wnt11 in anchorage-independent ...
Foretinib induces anoikis through a 2-step process. A, Hoechst 33342 staining of detached cells. CaOV3 cells were pretreated ... The inhibitor induces anoikis and blocks many functions important for ovarian cancer metastasis including, c-Met signaling, ... Our data suggest that anoikis induction contributes to the potent antitumor effects of the inhibitor. Characterization of the ... Consistent with a mechanism of anoikis, cell death occurred in 2 distinct stages; detachment followed by caspase-mediated ...
2d, e) cells after 48 h. Furthermore, through annexin V anoikis assay, we found that the knockdown of LMO3 promoted the anoikis ... Anoikis assays. 5 × 105 MHCC-97H or SMMC-7721 cells were cultured on poly-HEMA treated 12-well plates at 37 °C for 48 h. Then ... 6a, b). Meanwhile, the anoikis inhibition of Huh-7 or SNU-423 cells induced by rLMO3 protein was also abrogated by these ... LMO3 knockdown suppresses the invasion and anoikis inhibition of HCC cells in vitro. a Expression of LMO3 in HCC cell lines, ...
The results showed that knockdown of p27 had no effect on anoikis in EC9706 cells, suggesting the effect of SKP2 on anoikis in ... 28) proposed that galectin-3 inhibition of anoikis involves cell cycle arrest at an anoikis-insensitive point (late G1) through ... restored the ability of SKP2 to inhibit anoikis (Fig. 5A and B ). Next, we detected the effect of p27 on anoikis. As shown in ... Anoikis, a Greek word meaning loss of "home" or "homelessness," was originally defined by Frisch a decade ago as a unique ...
... anoikis explanation free. What is anoikis? Meaning of anoikis medical term. What does anoikis mean? ... Looking for online definition of anoikis in the Medical Dictionary? ... anoikis. Also found in: Wikipedia. anoikis. A type of programmed cell death (apoptosis) that is induced by a loss of correct ... anoikis. a special form of APOPTOSIS, whereby cells undergo cell death after disruption of cell-matrix interactions. Anoikis ...
Conclusions: MG-63 cells couldavoid anoikis through cell adhesion, and E-cadherin might play a role in this process. ... The aim of this study was to investigate the relationship between cell adhesion and anoikis evasionamong human osteosarcoma ... Conclusions: MG-63 cells couldavoid anoikis through cell adhesion, and E-cadherin might play a role in this process. ... "Correlation between E-Cadherin-Regulated Cell Adhesion and Human Osteosarcoma MG-63 Cell Anoikis". Asian Pacific Journal of ...
Acquisition of anoikis resistance in human osteosarcoma cells does not result in a generalized resistance to all apoptotic ... suspended). Moreover, suspended anoikis resistant TE-85 cells (TE-85ar) retained their sensitivity to chemotherapy as well. ... Moreover, our results suggest that the pathways regulating anoikis resistance and chemotherapy resistance might involve the ... anoikis) in human osteosarcoma would result in resistance to chemotherapy. Osteosarcoma cell lines (SAOS-2 and TE-85) obtained ...
Cucurbitacin I elicits anoikis sensitization, inhibits cellular invasion and in vivo tumor formation ability of nasopharyngeal ... However, when tumour cells detach they resist anoikis, allowing them to migrate to new sites and seed new tumours. The reasons ... STAT3 induces anoikis resistance, promotes cell invasion and metastatic potential in pancreatic cancer cells ... HIF-1 is induced via EGFR activation and mediates resistance to anoikis-like cell death under lipid rafts/caveolae-disrupting ...
  • The mechanism of inhibition by foretinib involved (a) inhibition of c-Met activation and downstream signaling, (b) reduction of ovarian cancer cell adhesion, (c) a block in migration and invasion, (d) reduced proliferation mediated by a G 2 -M cell-cycle arrest, and (e) induction of anoikis. (aacrjournals.org)
  • We show that mammary-specific stochastic inactivation of conditional E-cadherin and p53 results in impaired mammary gland function during pregnancy through the induction of anoikis resistance of mammary epithelium, resulting in loss of epithelial organization and a dysfunctional mammary gland. (biologists.org)
  • In vivo and in vitro experiments using the breast cancer cell lines MCF-7 and ZR-75-1, which expresses wild type p53, showed that tumorigenesis, colony formation, and anoikis resistance were significantly enhanced by MYBBP1A knockdown. (biomedcentral.com)
  • The inhibitors of the Hippo pathway abrogated rLMO3 protein-induced HCC cell invasion and anoikis inhibition. (springer.com)
  • These results suggest that LMO3 promotes HCC cell invasion and anoikis inhibition by interacting with LATS1 and suppressing Hippo signaling. (springer.com)
  • Therefore, understanding how normal HMECs overcome anoikis may provide insights into breast cancer initiation and progression. (beds.ac.uk)
  • In squamous cell carcinoma, researchers have found that anoikis resistance can be induced through hepatocyte growth factor (HGF) activating BOTH extracellular signalling-receptor kinase (ERK) and PI3K. (wikipedia.org)
  • Anoikis resistance can be induced through activation of extracellular signalling-receptor kinase (ERK) and the phosphatidylinositol 3-kinase (PI3K) signalling cascade by hepatocyte growth factor (HGF). (thefreedictionary.com)
  • Here, we provide evidence that B-RAF-MEK signaling protects against anoikis through alterations in two proapoptotic Bcl-2 family proteins: Bcl-xL/Bcl-2-associated death promoter (Bad) and Bcl-2-interacting mediator of cell death (Bim). (nih.gov)
  • In this study, we investigated the molecular mechanisms of a novel marine bacterial polysaccharide EPS11 which exerts its cytotoxic effects through affecting cancer cell adhesion and anoikis. (mdpi.com)
  • Mitogen-activated Protein/Extracellular Signal-regulated Kinase Kinase (MEK) Inhibitors Restore Anoikis Sensitivity in Human Breast Cancer Cell Lines with a Constitutively Activated Extracellular- regulated Kinase (ERK) Pathway 1 This work was supported by a Grant-in-Aid for Cancer Research from the Ministry of Education, Culture, Sports, Science, and Technology of Japan. (aacrjournals.org)
  • 2014). 'Correlation between E-Cadherin-Regulated Cell Adhesion and Human Osteosarcoma MG-63 Cell Anoikis', Asian Pacific Journal of Cancer Prevention , 15(19), pp. 8203-8207. (waocp.org)
  • Because both chemo- and anoikis-resistance are critical steps in the progression of ovarian cancer, we sought to determine how restoration of miR-200c affects tumor burden and chemosensitivity in an in vivo preclinical model of ovarian cancer. (aacrjournals.org)
  • Protein Kinase A Activation Promotes Cancer Cell Resistance to Glucose Starvation and Anoikis. (uni.lu)
  • Using omics and computational analyses, we found that cyclic adenosine monophosphate-Protein Kinase A (cAMP-PKA) axis activation is fundamental for cancer cell resistance to glucose starvation and anoikis. (uni.lu)
  • Since anoikis resistance plays a critical role in solid tumor growth, we investigated the relevance of these findings in the context of breast cancer. (beds.ac.uk)
  • However, the mechanisms underlying anoikis resistance in ovarian cancer are still unclear. (biomedcentral.com)
  • This most aggressive form of breast cancer didn't care - it had learned to be anoikis-resistant. (redorbit.com)
  • Thus, we assessed the effect of TGF-β1 on anoikis in established colorectal human cancer cell lines. (vanderbilt.edu)
  • Therefore, TGF-β paradoxically promotes the malignant behavior of a subset of TGF-β responsive colon cancer cell lines by blocking anoikis through cell-autonomous mechanisms. (vanderbilt.edu)
  • Hence, our data argue for a pivotal role for HIF-1α in anoikis control via suppression of α5 integrin. (aacrjournals.org)
  • Thus, our results suggest that EPS11 may be a potential candidate for human non-small cell lung carcinoma treatment via blocking filiform structure mediated adhesion and stimulating βIII-tubulin associated anoikis. (mdpi.com)
  • This resistant phenotype is stable and indicates that the processes of de-adhesion or exposure to a non-adhesive environment acts as a driving force towards anoikis resistance[ 18 ]. (biomedcentral.com)