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)
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 ...
Anoikis; and, in BLT2-overexpressing PWR-1E non-malignant prostate cells, 12(S)-HETE diminish anoikis-induced apoptosis. Thus, ... cascade following detachment confers anoikis resistance in prostate cancer cells". Journal of Biological Chemistry. 288 (42): ...
Patient derived xenograft
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 ...
"Human carcinoembryonic antigen functions as a general inhibitor of anoikis". Cancer Research. 60 (13): 3419-3424. PMID 10910050 ...
... contributes to tumor growth and protects cells from anoikis, a form of programmed cell death induced when contact- ... Terada LS, Nwariaku FE (March 2011). "Escaping Anoikis through ROS: ANGPTL4 controls integrin signaling through Nox1". Cancer ... March 2011). "Angiopoietin-like 4 protein elevates the prosurvival intracellular O2(-):H2O2 ratio and confers anoikis ...
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 ...
Eukaryotic translation elongation factor 1 alpha 1
... 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 ...
"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 ...
Anoikis Interstitium Perineuronal net Temporal feedback "Matrix - Definition and Examples - Biology Online Dictionary". 24 ...
"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 ...
Programmed cell death
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) ...
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- ...
"The HIV-1 vpr protein induces anoikis-resistance by modulating cell adhesion process and microfilament system assembly". Cell ...
Biology portal Anoikis Apaf-1 Apo2.7 Apoptotic DNA fragmentation Atromentin induces apoptosis in human leukemia U937 cells. ...
Some such forms of programmed cell death are anoikis, almost identical to apoptosis except in its induction; cornification, a ...
Matarrese P, Conti L, Varano B, Gauzzi MC, Belardelli F, Gessani S, Malorni W (2000). "The HIV-1 vpr protein induces anoikis- ...
... and anoikis". Molecular Biology Reports. 48 (11): 7545-7557. doi:10.1007/s11033-021-06706-1. ISSN 0301-4851. PMID 34519942. ... and anoikis". Molecular Biology Reports. 48 (11): 7545-7557. doi:10.1007/s11033-021-06706-1. PMID 34519942. S2CID 237506513. ...
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. Bibcode:2001Sci...293.1829P. doi:10.1126/science.1062257. PMID 11546872. ...
... activated by anoikis". Science. United States. 293 (5536): 1829-32. Bibcode:2001Sci...293.1829P. doi:10.1126/science.1062257. ... activated by anoikis". Science. 293 (5536): 1829-32. Bibcode:2001Sci...293.1829P. doi:10.1126/science.1062257. 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 ...
... activated by anoikis". Science. 293 (5536): 1829-32. Bibcode:2001Sci...293.1829P. doi:10.1126/science.1062257. PMID 11546872. ...
... causes anoikis resistance, chemoresistance and poor prognosis in ovarian cancer". Oncotarget. 7 (30): 47620-47636. doi:10.18632 ...
"Calreticulin promotes cell motility and enhances resistance to anoikis through STAT3-CTTN-Akt pathway in esophageal squamous ...
talks.cam : Anoikis and cell signalling in response to matrix attachment
Autophagy induction results in enhanced anoikis resistance in models of peritoneal disease<...
Autophagy induction results in enhanced anoikis resistance in models of peritoneal disease. Molecular Cancer Research. 2017 Jan ... Autophagy induction results in enhanced anoikis resistance in models of peritoneal disease. In: Molecular Cancer Research. 2017 ... Autophagy induction results in enhanced anoikis resistance in models of peritoneal disease. / Chen, James L.; David, Jason; ... Dive into the research topics of Autophagy induction results in enhanced anoikis resistance in models of peritoneal disease. ...
Mechanisms of Disease: the tissue kallikrein-kinin system in hypertension and vascular remodeling | Nature Reviews Nephrology
A novel RGD-independent cell adhesion pathway mediated by fibronectin-bound tissue transglutaminase rescues cells from anoikis ...
A novel RGD-independent cell adhesion pathway mediated by fibronectin-bound tissue transglutaminase rescues cells from anoikis ... A novel RGD-independent cell adhesion pathway mediated by fibronectin-bound tissue transglutaminase rescues cells from anoikis ... anoikis), suggesting an extracellular survival role for tTG. We propose a novel RGD-independent cell adhesion mechanism that ...
A role for PVRL4-driven cell-cell interactions in tumorigenesis | eLife
Anchorage-independent colony formation and anoikis assays. Request a detailed protocol Anchorage-independent colony formation ... Mammary epithelial cells are known to undergo an alternative anoikis-related cell death program characterized by robust ... For anoikis assays, cells were seeded on ultra-low attachment dishes (Corning, Midland, MI) in reduced growth factor MEGM with ... loss of contact with the proper ECM molecules results in initiation of a cell death program known as anoikis (Frisch and ...
Comprehensive analysis of anoikis-related long non-coding RNA immune infiltration in patients with bladder cancer and...
Anoikis is a form of programmed cell death or programmed cell death(PCD) for short. Studies suggest that anoikis involves in ... We sought to screen for anoikis-correlated long non-coding RNA (lncRNA) so that we can build a risk model to understand its ... We screened seven anoikis-related lncRNAs (arlncRNAs) from The Cancer Genome Atlas (TCGA) and designed a risk model. It was ... Comprehensive analysis of anoikis-related long non-coding RNA immune infiltration in patients with bladder cancer and ...
MYBBP1A MYB binding protein 1a [Homo sapiens (human)] - Gene - NCBI
Mian Shahzad | Moffitt
The AMEDEO Literature Guide
Ming Liu - Search Results - PubMed
Activation of NF-E2-Related Factor-2 Reverses Biochemical Dysfunction of Endothelial Cells Induced by Hyperglycemia Linked to...
Cell death: Is our health at risk?
Asha S. Multani | MD Anderson Cancer Center
Targeting YAP-Dependent MDSC Infiltration Impairs Tumor Progression | Cancer Discovery | American Association for Cancer...
Specifically, Hippo pathway components LATS1/2 have been implicated in anoikis and metastasis in prostate cancer (28), and ERG- ... Cell detachment activates the Hippo pathway via cytoskeleton reorganization to induce anoikis ... and is implicated in the regulation of anoikis and metastasis in prostate cancer (28) and the development of age-related ...
The epithelial-mesenchymal transition: new insights in signaling, development, and disease | Journal of Cell Biology |...
PKC Alpha antibody (21991-1-AP) | Proteintech
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KatiaSae - Signal Cartel
THE ANOIKIS DIVISION. Manager: Tamayo. General Information. As of 24 March 2021, I am pleased to report that the division is ... Beacon of Anoikis ( 100 rescues) - Xalyar, Captain Crinkle. And as always a huge thanks to A Dead Parrot and Allison. They are ... The Anoikis Division has a great core group of excellent and enthusiastic pilots. Many of which contribute to the success of ... After so long in Empire space, the silence of Anoikis was ominous as I imagined cloaked hunters closing in on all sides, ready ...
Potassium channels as novel molecular targets in hepatocellular carcinoma (Review)
I am a medical oncologist specializing in the care of patients with breast cancer. As a physician-scientist, I also lead a research laboratory that is focused on developing targeted therapies tailored for specific breast cancer subtypes and for individual patients. I have a particular interest in better understanding triple negative breast cancers, with the goal of integrating genetic analysis to the development of improved treatments for our patients. I am co-PI of the Breast Tumor Biospecimen Repository, which is a bank of patient breast tumors; analysis of these tumors will provide insights into the genetic changes that determine sensitivity to specific targeted therapies for breast cancer. I am also co-PI of a study investigating the use of patient-derived xenograft models as a model for chemotherapy treatment sensitivity for patients with triple negative breast cancers; if successful, these models may be used in the future to help us better tailor treatments for individual patients. My ...
Has suicide ganking become a problem? Empty freighters being ganked. - EVE General Discussion - EVE Online Forums
Carrie Elzie - Producción científica - Scholars @ UT Health San Antonio
Ca2+-ATPase - High-Throughput Screen for the Chemical Inhibitors
Michael A White - Research output - University of Texas Southwestern Medical Center
Freeman-Cook, K., Hoffman, R. L., Miller, N., Almaden, J., Chionis, J., Zhang, Q., Eisele, K., Liu, C., Zhang, C., Huser, N., Nguyen, L., Costa-Jones, C., Niessen, S., Carelli, J., Lapek, J., Weinrich, S. L., Wei, P., McMillan, E., Wilson, E., Wang, T. S., & 28 othersMcTigue, M., Ferre, R. A., He, Y. A., Ninkovic, S., Behenna, D., Tran, K. T., Sutton, S., Nagata, A., Ornelas, M. A., Kephart, S. E., Zehnder, L. R., Murray, B., Xu, M., Solowiej, J. E., Visswanathan, R., Boras, B., Looper, D., Lee, N., Bienkowska, J. R., Zhu, Z., Kan, Z., Ding, Y., Mu, X. J., Oderup, C., Salek-Ardakani, S., White, M. A., VanArsdale, T. & Dann, S. G., Oct 11 2021, In: Cancer Cell. 39, 10, p. 1404-1421.e11. Research output: Contribution to journal › Article › peer-review ...
Kentaro Semba - Research output - Waseda University
Nakamura, T., Hashikawa, C., Okabe, K., Yokote, Y., Chirifu, M., Toma-Fukai, S., Nakamura, N., Matsuo, M., Kamikariya, M., Okamoto, Y., Gohda, J., Akiyama, T., Semba, K., Ikemizu, S., Otsuka, M., Inoue, J. I. & Yamagata, Y., 2020 Dec 1, In: Scientific reports. 10, 1, 5152.. Research output: Contribution to journal › Article › peer-review ...
DeCS - New terms
- To identify potential therapies, we developed in vitro models of peritoneal carcinomatosis/peritoneal sarcomatosis using tumor cell lines and patient-derived spheroids (PDS) that recapitulate anoikis resistance and spheroid proliferation across multiple cancer types. (elsevierpure.com)
- Aspirin Suppresses Breast Cancer Metastasis to Lung by Targeting Anoikis Resistance. (amedeo.com)
- These cells also showed increased sphere formation, anoikis resistance, and aldehyde dehydrogenase (ALDH) activities, which are characteristics of stem cells. (cdc.gov)
- The tTG-FN complex can maintain cell viability of tTG-null mouse dermal fibroblasts when apoptosis is induced by inhibition of RGD-dependent adhesion (anoikis), suggesting an extracellular survival role for tTG. (ntu.ac.uk)
- Comprehensive analysis of anoikis-related long non-coding RNA immune infiltration in patients with bladder cancer and immunotherapy. (bvsalud.org)
- Studies suggest that anoikis involves in the decisive steps of tumor progression and cancer cell metastasis and spread, but what part it plays in bladder cancer remains unclear. (bvsalud.org)
- We sought to screen for anoikis -correlated long non-coding RNA ( lncRNA ) so that we can build a risk model to understand its ability to predict bladder cancer prognosis and the immune landscape. (bvsalud.org)
- We screened seven anoikis -related lncRNAs (arlncRNAs) from The Cancer Genome Atlas (TCGA) and designed a risk model. (bvsalud.org)
- Anoikis is a form of programmed cell death or programmed cell death (PCD) for short. (bvsalud.org)
- Bit1 is a mitochondrial protein that induces a caspase-independent apoptosis upon its release into the cyto sol following loss of integrin-mediated attachment to extracellular matrix (anoikis). (scirp.org)
- Mecha nistically, we found that the Bit1 apoptosis function is in part dependent on the groucho related Amino-terminal En hancer of Split (AES) expression and is abrogated by the transcriptional corepressor TLE1 protein. (scirp.org)
- K. Leleux, T. Pham, M. Davis, P. Karmali and H. Biliran, "Induction of Apoptosis and Anoikis by Bit1 in Pancreatic Cancer Cells," Journal of Cancer Therapy , Vol. 4 No. 4, 2013, pp. 815-824. (scirp.org)
- The loss of cell-matrix interactions induces apoptosis, known as anoikis. (nih.gov)
- Incidentally, because VLA-4 interacts with fibronectin at a different site than the one at which it interacts with VCAM-1 (ref. 25), the differences in signaling may explain why the VCAM-1-VLA-4 interaction did not induce resistance to anoikis or drug-induced apoptosis. (medscape.com)
Resistance to anoikis1
- TGFBR3 loss promotes cell survival through resistance to anoikis. (biologists.com)
- To find al ternative cell death pathways that can bypass the apoptotic resistance of pancreatic cancer cells, we examined the role of the novel anoikis effector Bit1 (Bcl-2 inhibitor of transcription) in the survival and apoptotic resistance of pancreatic cancer cells. (scirp.org)
- 1. Identification of a novel anoikis signalling pathway using the fungal virulence factor gliotoxin. (nih.gov)
- TGF-beta has paradoxical and context dependent effects on proliferation and anoikis in human colorectal cancer cell lines. (nih.gov)
- We investigated the effect of TGF-beta on anoikis in colorectal cancer cell lines sensitive to TGF-beta-mediated growth inhibition to determine if the context of the cells could be one of the factors that would affect whether TGF-beta exerts tumor suppressor or oncogene activity on colon cancer cells. (nih.gov)
- 3. An altered fibronectin matrix induces anoikis of human squamous cell carcinoma cells by suppressing integrin alpha v levels and phosphorylation of FAK and ERK. (nih.gov)
- 5. Integrin endosomal signalling suppresses anoikis. (nih.gov)
- 7. Squamous cell carcinoma cell aggregates escape suspension-induced, p53-mediated anoikis: fibronectin and integrin alphav mediate survival signals through focal adhesion kinase. (nih.gov)
- 8. Delayed caspase-8 activation and enhanced integrin β1-activated FAK underpins anoikis in oesophageal carcinoma cells harbouring mt p53-R175H. (nih.gov)
- 10. NG2, a novel proapoptotic receptor, opposes integrin alpha4 to mediate anoikis through PKCalpha-dependent suppression of FAK phosphorylation. (nih.gov)
- 19. HPW-RX40 restores anoikis sensitivity of human breast cancer cells by inhibiting integrin/FAK signaling. (nih.gov)
- Moreover, we reported that FxOH rapidly detached human CRC cells (DLD-1 cell line) from a culture dish and induced anoikis-like cell death through the suppression of integrin β1 and inactivation of focal adhesion kinase [ 10 ]. (biomedcentral.com)
- 11. Combinatorial activation of FAK and AKT by transforming growth factor-beta1 confers an anoikis-resistant phenotype to myofibroblasts. (nih.gov)
- For successful distant metastasis, circulating tumor cells (CTCs) that have lost matrix attachment need to acquire anoikis resistance in order to survive. (nih.gov)
- 17. Akt and RhoA inhibition promotes anoikis of aggregated B16F10 melanoma cells. (nih.gov)
- 20. Acquisition of anoikis resistance promotes alterations in the Ras/ERK and PI3K/Akt signaling pathways and matrix remodeling in endothelial cells. (nih.gov)
- We observed variable effects of TGF-beta on anoikis in these cell lines, even though they all are growth-inhibited by TGF-beta. (nih.gov)
- The mechanism for anoikis resistance almost certainly differs between cell types. (medscape.com)
- 14. Redox regulation of anoikis: reactive oxygen species as essential mediators of cell survival. (nih.gov)
- 16. G1/S cell cycle arrest provides anoikis resistance through Erk-mediated Bim suppression. (nih.gov)
- Conversely, downregulation of endogenous Bit1 in PANC-1 cells further enhanced their anoikis resistance. (scirp.org)
- These cells also showed increased sphere formation, anoikis resistance, and aldehyde dehydrogenase (ALDH) activities, which are characteristics of stem cells. (cdc.gov)
- The chronic CNM-exposed cells exhibited CSC-like properties as indicated by 3D spheroid formation, anoikis resistance, and CSC marker expression. (cdc.gov)