• The structure of CDKs in complex with a cyclin subunits (CDKC) has long been a goal of structural and cellular biologists starting in the 1990s when the structure of unbound cyclin A was solved by Brown et al. (wikipedia.org)
  • These cyclin binding sites are the regions of highest variability in CDKs despite relatively high sequence homology surrounding the αL-12 Helix motif of this structural component. (wikipedia.org)
  • Passage through the cell cycle requires the successive activation of different cyclin-dependent protein kinases (CDKs). (unibas.ch)
  • Cyclin dependent kinases (CDKs) phosphorylate several substrates such as transcription factors and cytoskeletal proteins, which leads to the transition of the cell into the next cell cycle phase. (onkoview.com)
  • CDKs are activated by cyclins, which are expressed in distinct phases during the cell cycle. (onkoview.com)
  • Importantly, CDKs are inhibited by specific cyclin dependent kinase inhibitors. (onkoview.com)
  • By default, CDKs are always present in a cell in an inactivated form. (jove.com)
  • Thus, levels of the four different cyclins vary in predictable patterns and combine with consistent CDKs at specific points to achieve forward momentum. (jove.com)
  • Positive regulators include two protein groups that allow cells to pass through regulatory checkpoints: cyclins and cyclin-dependent kinases (CDKs). (jove.com)
  • Cyclin-dependent kinases (CDKs) are serine/threonine protein kinases that act as key regulatory elements in cell cycle progression. (rcsb.org)
  • The profiling of compound 51 against a panel of 339 kinases revealed high selectivity for CDKs, with preference for CDK2 and CDK5 over CDK9, CDK1, CDK4, and CDK6. (rcsb.org)
  • Progression through the cell cycle is driven by the oscillating activity of Cyclin Dependent Kinases (CDKs). (intechopen.com)
  • The activity of CDKs is controlled by their binding to coactivator subunits termed Cyclins, as well as by CDK inhibitory proteins termed CKIs. (intechopen.com)
  • Cyclin-dependent kinases (Cdks) are principal drivers of cell division and are an important therapeutic target to inhibit aberrant proliferation. (escholarship.org)
  • Cancer cells exploit Spy1 to stimulate proliferation through inappropriate activation of Cdks, yet the mechanism is unknown. (escholarship.org)
  • The cyclin-dependent kinase (CDK) inhibitors p21 and p16 inhibit the activity of CDKs, such as CDK4. (medscape.com)
  • As a biologically important example we have studied the complex formed by cyclins and cyclin-dependent kinases (CDKs), which play an essential role in the control of the eukaryotic cell cycle. (lu.se)
  • They further link to the activation of protein kinase C- (PKC-) induced generation of reactive oxygen species (ROS) [ 6 , 7 ], which further mediates the activation of downstream transcription factor nuclear factor kappa-light-chain enhancer of activated B cells (NF- κ B). Thus, the main treatments of DN refer to modulate glycemic and blood pressure through insulin and RAS inhibitors. (hindawi.com)
  • Although the senescent cells remain viable, they show typical changes with enlarged and flattened cell bodies, apoptosis resistance, increased activity of senescence-associated β -galactosidase (SA- β -gal), and upregulation of cyclin-dependent kinase (CDK) inhibitors including p16 INK4A , ARF proteins, and p21 [ 13 - 16 ]. (hindawi.com)
  • [ 2 ] Options for second-line therapy in patients with relapsed/refractory disease include chemotherapy-free regimens with biologic targeted agents such as covalent Bruton tyrosine kinase (BTK) inhibitors, lenalidomide,venetoclax, and chimeric antigen receptor (CAR) T-cell therapy. (medscape.com)
  • Polo-like kinase (PLK) inhibitors targets the mitotic phase of the cell cycle. (pharmaceutical-technology.com)
  • The activity of this kinase first appears in mid-G1 phase, which is controlled by the regulatory subunits including D-type cyclins and members of INK4 family of CDK inhibitors. (cancerindex.org)
  • Novel Plant-specific cyclin-dependent kinase inhibitors induced by biotic and abiotic stresses. (helsinki.fi)
  • Cdk enzymatic activity is tightly controlled through cyclin interactions, posttranslational modifications, and binding of inhibitors such as the p27 tumor suppressor protein. (escholarship.org)
  • Another important class of tumor suppressor genes involved in cell cycle control and in the generation of human cancers is the cyclin-dependent kinase (CDK) inhibitors. (medscape.com)
  • A cyclin-dependent kinase complex (CDKC, cyclin-CDK) is a protein complex formed by the association of an inactive catalytic subunit of a protein kinase, cyclin-dependent kinase (CDK), with a regulatory subunit, cyclin. (wikipedia.org)
  • Diagnostic subsets of coexpressed genes reflected signaling activity, cross talk, and overlap of multiple mitogen-activated protein kinase (MAPK) pathways. (nih.gov)
  • This kinase is a catalytic subunit of the protein kinase complex that is important for cell cycle G1 phase progression and G1/S transition. (cancerindex.org)
  • Activation of the MCM complex at origins by cyclin-dependent kinases and the CDC7 protein kinase (P06243) leads to initiation of DNA synthesis. (yeastgenome.org)
  • It is at this essential residue (T160 in CDK2 complexes, T177 in CDK6 complexes) that enzymatic ATP-phosphorylation of CDK-cyclin complexes by CAK (cyclin activating kinase, referring to the CDK7-Cyclin H complex in human cells) takes place. (wikipedia.org)
  • The regulatory region is subject to differential phosphorylation at non-glycine residues within this motif, making this site subject to Wee1 and/or Myt1 inhibitory kinase phosphorylation and Cdc25 de-phosphorylation in mammals. (wikipedia.org)
  • Study of this residue has shown that phosphorylation promotes a conformational change that prevents ATP and substrate binding by steric interference with these necessary binding sites in the activation loop of the CDK-cyclin complexes. (wikipedia.org)
  • Thus, this hinge region, which can vary in length slightly between CDK type and CDK-cyclin complex, connects essential regulatory regions of the CDK by connecting these lobes, and plays key roles in the resulting structure of CDK-cyclin complexes by properly orienting ATP for easy catalysis of phosphorylation reactions by the assembled complex. (wikipedia.org)
  • These enzymes are controlled by transient associations with cyclin regulatory subunits, binding of inhibitory polypeptides and reversible phosphorylation reactions. (unibas.ch)
  • Subsequently, a different set of CDK/cyclin complexes triggers the phosphorylation of numerous proteins to promote the profound structural reorganizations that accompany the entry of cells into mitosis. (unibas.ch)
  • G 2 /M arrest was associated with DNA damage as indicated by phosphorylation of H 2 A.X at Ser139 and activation of checkpoint kinase 2 (Chk2) in all the three cell lines. (aspetjournals.org)
  • Compound 51 inhibited the proliferation of 13 out of 15 cancer cell lines with IC50 values between 0.27 and 6.9 μM, which correlated with the complete suppression of retinoblastoma phosphorylation and the onset of apoptosis. (rcsb.org)
  • This phosphorylation event is associated with increased cell proliferation and poor prognosis in patients with glioma. (umass.edu)
  • Treatment of breast cancer cell lines with the combination of palbociclib and antiestrogens leads to decreased retinoblastoma protein (Rb) phosphorylation resulting in reduced E2F expression and signaling and increased growth arrest compared to treatment with each drug alone. (shu.edu)
  • Virtually all mitogenic signals to the cell are processed through CDK4/6 - it is truly the central molecule that governs pRb phosphorylation status up through the R-point transition. (shu.edu)
  • During early G1 phase, mitogenic signals trigger activation of the CDK4/6-cyclin D complex, which partially deactivates Rb by phosphorylation. (shu.edu)
  • Apoptosis-related protein-1 acts as a tumor suppressor in cholangiocarcinoma cells by inducing cell cycle arrest via downregulation of cyclin-dependent kinase subunits. (nih.gov)
  • solved the structure of human cyclin A-CDK2 complex to 2.3 Angstrom resolution. (wikipedia.org)
  • Expression of cell-cycle regulator CDK2-associating protein 1 (p12CDK2AP1) in transgenic mice induces testicular and ovarian atrophy in vivo. (nih.gov)
  • Cyclin dependent-kinase 2 (CDK2) plays important functions during the mitotic cell cycle and also facilitates several key events during germ cell development. (lu.se)
  • A better understanding of the CDK2 substrates will help us to gain deeper insight into the functions of this universal kinase. (lu.se)
  • In order to enter S phase, cells must sequentially activate CDK4/6 and CDK2. (shu.edu)
  • Activation of the CDK2-cyclin E complex results in hyperphosphorylation of Rb and fully releases E2F. (shu.edu)
  • We identify mutations in Spy1 that ablate its ability to activate Cdk2 and to proliferate cells. (escholarship.org)
  • Internal regulatory checkpoints ensure that a cell's size, energy reserves, and DNA quality and completeness are sufficient to advance through the cell cycle. (jove.com)
  • At these checkpoints, positive and negative regulators promote or inhibit a cell's continuation through the cell cycle. (jove.com)
  • Spy1/RINGO (Spy1) proteins bind and activate Cdk but are resistant to canonical regulatory mechanisms that establish cell-cycle checkpoints. (escholarship.org)
  • Resveratrol could play a toxic role through inducing apoptosis of the cancer cell in a time- and concentration-dependent manner. (mdpi.com)
  • The p53 protein is an important tumor suppressor that is essential for regulating cell division, senescence, and self-destruction (apoptosis). (medlineplus.gov)
  • Blocking ROS generation by N -acetyl cysteine protects the cells from DIM-mediated G 2 /M arrest and apoptosis. (aspetjournals.org)
  • The encoded protein is likely associated with apoptosis, cell cycle arrest, growth inhibition or cell differentiation. (nih.gov)
  • JAM3 knockdown additionally inhibited trophoblast proliferation and increased the number of trophoblasts in the sub-G1 and G2/M phases, indicating cell-cycle disturbance and apoptosis. (bioone.org)
  • Ectopic Mcl-1 expression attenuates Bak activation and apoptosis by ABT-737 + roscovitine, whereas cells overexpressing Bcl-2 or Bcl-xL remain fully sensitive. (aacrjournals.org)
  • HA14-1) that disable Bcl-2, resulting in induction of apoptosis in leukemia cell lines ( 8 ). (aacrjournals.org)
  • The TP53 gene is also capable of stimulating apoptosis of cells containing damaged DNA. (medscape.com)
  • TP53 activates the expression of genes involved in apoptosis, cell cycle regulation (p21), and MDM2. (medscape.com)
  • When this complex forms the CDK can phosphorylate a target protein which alters it's function and initiates the cell to advance to the next phase. (jove.com)
  • This kinase, as well as CDK4, has been shown to phosphorylate, and thus regulate the activity of, tumor suppressor protein Rb. (cancerindex.org)
  • CDK4 and CDK6 normally stimulate the cell to continue through the cycle and divide. (medlineplus.gov)
  • Cyclin D1 and CDK4/6 are downstream of signaling pathways which lead to cellular proliferation. (shu.edu)
  • The p16INK4A protein is a cell-cycle inhibitor that acts by inhibiting activated cyclin D:CDK4/6 complexes, which play a crucial role in the control of the cell cycle by phosphorylating Rb protein. (medscape.com)
  • Cyclin-dependent kinase 2-associating protein 1 commits murine embryonic stem cell differentiation through retinoblastoma protein regulation. (nih.gov)
  • Cyclin dependent kinases are a key family of kinases involved in cell cycle regulation and are an attractive target for cancer chemotherapy. (rcsb.org)
  • Here, we show that Mcl-1 down-regulation by the cyclin-dependent kinase (CDK) inhibitor roscovitine or Mcl-1-shRNA dramatically increases ABT-737 lethality in human leukemia cells. (aacrjournals.org)
  • The Arabidopsis thaliana homolog of yeast BRE1 has a function in cell cycle regulation during early leaf and root growth. (helsinki.fi)
  • They must bind to a specific cyclin to be activated. (jove.com)
  • In this way, p16(INK4A) controls cell division. (medlineplus.gov)
  • Cells begin to produce p16(INK4A) when they are no longer able to undergo cell division. (medlineplus.gov)
  • Without p16(INK4A) to regulate cell growth and division (proliferation), cells can continue to grow and divide without control, which can lead to tumor formation. (medlineplus.gov)
  • CDKN2A gene mutations involved in cancer impair production of functional p16(INK4A) or, less commonly, p14(ARF), which can result in uncontrolled cell growth and tumor formation. (medlineplus.gov)
  • Our studies show that after being secreted into the extracellular matrix, CCN5 binds to the α6β1 integrins of the cells leading to inhibition of the PI3K-AKT signaling pathway. (ku.edu)
  • p27, cyclin D1, and retinoblastoma (Rb) protein have been demonstrated using immunohistochemistry in 189 cases of primary breast carcinoma with long-term follow-up. (ox.ac.uk)
  • There was a statistically significant association between the expression of p27 and both cyclin D1 and the retinoblastoma gene product (pRb), corresponding to their close interactions in regulating the G1/S transition in the cell cycle. (ox.ac.uk)
  • In future, a better understanding of the cell cycle machinery and its deregulation during oncogenesis may provide novel opportunities for the diagnostic and therapeutic management of cancer and other proliferation-related diseases. (unibas.ch)
  • MAGEH1 reduced HCC cell proliferation, migration and invasion ability. (nih.gov)
  • Previous researches completed by our team have also demonstrated that resveratrol inhibits the proliferation, invasion, and metastasis of colorectal cancer cells [ 5 ]. (hindawi.com)
  • Notably, the G1/S boundary represents a major barrier to cell proliferation and is universally dysfunctional in cancer cells, allowing for the unbridled proliferation observed in malignancy. (intechopen.com)
  • Numerous E3 ubiquitin ligases, which facilitate the ubiquitination of specific substrates, have been shown to control G1/S. In this chapter, we will discuss components in the ubiquitin proteasome system that are implicated in G1/S control, how these enzymes are interconnected, gaps in our current knowledge, and the potential role of these pathways in the cancer cycle and disease proliferation. (intechopen.com)
  • A mutation in this gene resulting in reduced cell proliferation, and impaired cell motility and polarity, and has been identified in patients with primary microcephaly. (cancerindex.org)
  • The bioactive compound of Kencur ginger, ethyl p-methoxycinnamate, reduces cancer cell proliferation in mice. (technologynetworks.com)
  • In mice, this compound reduced cancer cell proliferation at low doses. (technologynetworks.com)
  • It was thought to decrease the expression of a protein called mitochondrial transcription factor A (TFAM), a key player in cancer cell proliferation. (technologynetworks.com)
  • Inactivation of tumor suppressor genes, whose products normally provide negative control of cell proliferation, contributes to malignant transformation in various cell types. (medscape.com)
  • At present, much research is focused on elucidating the links between CDK/cyclin complexes and signal transduction pathways controlling cell growth, differentiation and death. (unibas.ch)
  • Neuronal differentiation and cell-cycle programs mediate response to BET-bromodomain inhibition in MYC-driven medulloblastoma. (cancerindex.org)
  • Cell-cycle arrest was associated with the engagement of checkpoint kinase 2-cell division cycle 25C-cyclin-dependent kinase 1/cyclin B1 signaling. (bioone.org)
  • E is then degraded by cytoplasmic enzymes and cyclin A concentrations increase throughout the S phase and remain high into G2 to promote entry into the M phase when in an active complex. (jove.com)
  • In my own field, membrane trafficking, the premier example was the pancreatic acinar cell from guinea pigs ( Fig. 1 ), which is responsible for secreting (in a regulated fashion) those digestive enzymes needed after food digested in the stomach enters the small intestine. (rupress.org)
  • This cell devotes up to 70% of its total protein synthetic capacity to producing these enzymes. (rupress.org)
  • Furthermore, this is an architecturally elegant cell, with the ER at the base (beneath and around the nucleus), the Golgi just above the nucleus, and the maturing secretory granules just above that, providing a clear map that could be used to plot the movement of newly synthesized enzymes ( Fig. 1 ). (rupress.org)
  • Cyclin-dependent kinase inhibitor p27Kip1 expression and interaction with other cell cycle-associated proteins in mammary carcinoma. (ox.ac.uk)
  • This leads to stabilization and nuclear localization of FOXO3A resulting in transcriptional activation of the cyclin-dependent kinase inhibitor P27KIP1. (ku.edu)
  • Also, we found that the CCN5-induced PI3K-AKT inactivation leads to stabilization and nuclear accumulation of P27KIP1 resulting in cell cycle arrest of TNBC cells. (ku.edu)
  • MEN 4 is caused by an inactivating mutation of the CDKN1B gene, which codes for the cyclin dependent kinase inhibitor 1B protein, also known as p27 or p27KIP1. (msdmanuals.com)
  • In many types of cancer, proteins that regulate the cell cycle are deregulated by genetic or epigenetic changes in the corresponding genes. (onkoview.com)
  • Somatic mutations in other genes involved in cell growth are also needed for a melanoma to develop. (medlineplus.gov)
  • Subsequently released E2F factors mediate expression of pro-proliferative genes including cyclin E and Cdc25A. (shu.edu)
  • Eukaryotic expression vectors containing genes encoding plant proteins for killing of cancer cells. (weeksmd.com)
  • consequently, genes encoding some of these proteins are being used to design constructs for the inhibition of multiplying cancer cells. (weeksmd.com)
  • Results: Data addressing the function of vectors harbouring genes specifically encoding ricin, saporin, lunasin , linamarase, and tomato thymidine kinase 1 under the control of different promoters are summarised here. (weeksmd.com)
  • Like Rb protein, many of the proteins encoded by tumor suppressor genes act at specific points in the cell cycle. (medscape.com)
  • High resolution structures exist for approximately 25 CDK-cyclin complexes in total within the Protein Data Bank. (wikipedia.org)
  • The difference between the forms lies within the binding of cyclin partners where closed form complexes have CDK-cyclin binding at both the C and N-termini of the activation loop of the CDK, whereas the open form partners bind only at the N-terminus. (wikipedia.org)
  • p27 regulates G1 /S transition by abrogating the activity of cyclin/CDK complexes. (umass.edu)
  • Growth-inhibitory effects of DIM were mediated by cell cycle arrest in G 2 /M phase in all the three cell lines. (aspetjournals.org)
  • To further establish the involvement of Chk2 in DIM-mediated G 2 /M arrest, cells were transfected with dominant-negative Chk2 (DN-Chk2). (aspetjournals.org)
  • Blocking Chk2 activation by DN-Chk2 completely protected cells from DIM-mediated G 2 /M arrest. (aspetjournals.org)
  • These results were further confirmed in Chk2 knockout DT40 lymphoma cells, in which DIM failed to cause cell cycle arrest. (aspetjournals.org)
  • These results clearly indicate the requirement of Chk2 activation to cause G 2 /M arrest by DIM in ovarian cancer cells. (aspetjournals.org)
  • Here, we have shown that Cysteine-rich 61-Connective Tissue Growth Factor-nephroblastoma-overexpressed 5 (CCN5) induces growth arrest of TNBC cells in-vitro and in xenograft tumors. (ku.edu)
  • Initial observations indicate that CCN5 induces expression of P16INK4A and P19ARF, resulting in cell cycle arrest of the tumor cells. (ku.edu)
  • Activation of p21 or p16 therefore causes cell cycle arrest. (medscape.com)
  • The p19ARF protein, which is encoded by the same locus as p16, also leads to cell cycle arrest by inhibiting the ability of MDM2 to inactivate TP53. (medscape.com)
  • Major histocompatibility complex class I (MHC I) molecules present antigenic peptides to cytotoxic T cells to eliminate infected or cancerous cells. (researchgate.net)
  • The conserved hinge region of CDK within eukaryotic cells acts as an essential bridge between the Gly-rich loop and the activation loop. (wikipedia.org)
  • Essential for 'once per cell cycle' DNA replication initiation and elongation in eukaryotic cells, associates with the origins of DNA replication to form part of the pre-replicative complex. (yeastgenome.org)
  • Thereafter, a distinct subpopulation of endothelial cells lining the cardinal vein starts differentiating by expressing the TF PROX1, the master regulator of lymphatic endothelial cell (LEC) identity, via the TFs SOX18 and COUPTFII. (nature.com)
  • S-phase kinase-associated protein 2 (SKP2) is an important cell cycle regulator, targeting the cyclin-dependent kinase (CDK) inhibitor p27 for degradation, and is frequently overexpressed in breast cancer. (umass.edu)
  • Cyclin-dependent kinase 4 is a key regulator of G1 PHASE of the CELL CYCLE. (bvsalud.org)
  • Some treatments target specific characteristics of cancer cells, so they only work on those particular cancers. (healthline.com)
  • Lack of ER-α expression in TNBC cells or loss of ER-α activation after endocrine treatment of luminal cancers makes these breast cancer cells resistant to tamoxifen and other endocrine therapies. (ku.edu)
  • Spy1 lacks the cyclin-binding site that mediates p27 and substrate affinity, explaining why Cdk-Spy1 is poorly inhibited by p27 and lacks specificity for substrates with cyclin-docking sites. (escholarship.org)
  • A cells cycle is positively regulated promoting progress through the stages via the interaction of two classes of proteins found in the cytoplasm. (jove.com)
  • Mutations in the CDKN2A gene are found in up to one-quarter of head and neck squamous cell carcinomas (HNSCC). (medlineplus.gov)
  • Mutations in the CDKN2A gene are also associated with melanoma, a type of skin cancer that begins in pigment-producing cells called melanocytes. (medlineplus.gov)
  • For instance, during G1, when one type of cyclin, named D, is synthesized and binds to a CDK, the cell transitions into S phase, as another cyclin, E, peaks and forms a complex with CDK to promote DNA replication. (jove.com)
  • It acts as a tumor suppressor and when the protein is lost, cells can undergo unscheduled replication, which may eventually lead to cancer. (msdmanuals.com)
  • The interest in p27 expression in mammary carcinoma lies in its behaviour when examined in combination with other G1 cell cycle regulators. (ox.ac.uk)
  • It is important to note that in CDK 1, 2 and 6, the T-loop and a separate C-terminal region are the major sites of cyclin binding in the CDK, and which cyclins are bound to each of these CDK is mediated by the particular sequence of the activation site T-loop. (wikipedia.org)
  • This activity is aided by the notable flexibility that the Gly-rich loop has within the structure of most CDK allowing for its rotation toward the activation loop to have a significant effect on reducing substrate affinity without major changes in the overall CDK-cyclin complex structure. (wikipedia.org)
  • Activation of the VEGFA/VEGFR2 signaling and expression of blood vascular endothelial cell (BEC) markers, such as NRP1 and EphrinB2, further differentiate these precursor cells into BECs, which then form the hierarchical network of blood vessels 4 . (nature.com)
  • Assay of the mutants with a cyclin-dependent kinase 4-selective bisanilinopyrimidine shows that the K89T mutation is primarily responsible for the selectivity of this compound. (rcsb.org)
  • Use of the cyclin-dependent kinase 2-selective 6-cyclohexylmethoxy-2-(4'-sulfamoylanilino)purine (NU6102) shows that K89T has no role in the selectivity, while the remaining three mutations have a cumulative influence. (rcsb.org)
  • The accumulation of both Cyclin and CKI proteins is tightly regulated at the level of transcription. (intechopen.com)
  • During development, the blood vascular system arises from endothelial cell progenitors that differentiate from mesodermal cells, mostly through the expression of the transcription factor (TF) ETV2. (nature.com)
  • As a transcription factor whose expression is increased by DNA damage, p53 blocks cell division at the G1 phase of the cell cycle to allow DNA repair. (medscape.com)
  • In most cases, when a cyclin is degraded, the CDK is inactivated, signaling the end of a particular phase. (jove.com)
  • After A is degraded, concentrations of cyclin B peak in M phase and the complex will activate the different stages of mitosis. (jove.com)
  • Cyclins can be categorized as G 1 , G 1 /S, S, or M cyclins based on the cell cycle phase or transition they are most involved in. (jove.com)
  • Plogosertib is under clinical development by Cyclacel Pharmaceuticals and currently in Phase II for Diffuse Large B-Cell Lymphoma. (pharmaceutical-technology.com)
  • According to GlobalData, Phase II drugs for Diffuse Large B-Cell Lymphoma have a 40% phase transition success rate (PTSR) indication benchmark for progressing into Phase III. (pharmaceutical-technology.com)
  • This transfers cells past the restriction (R) point, which commits for S-phase entry. (shu.edu)
  • In this study, by comparing the activity of normal cell lines and cancer cell lines after treating with resveratrol, it was found that resveratrol has more significant cytotoxicity in cancer cell lines. (mdpi.com)
  • Without one of these tumor suppressors, cells can grow and divide unchecked, leading to the development of cancer. (medlineplus.gov)
  • We evaluated the effect of 3,3′-diindolylmethane (DIM) in ovarian cancer cells. (aspetjournals.org)
  • DIM treatment inhibited the growth of SKOV-3, TOV-21G, and OVCAR-3 ovarian cancer cells in both a dose- and time-dependent manner with effective concentrations ranging from 40 to 100 μM. (aspetjournals.org)
  • Our results establish Chk2 as a potent molecular target of DIM in ovarian cancer cells and provide the rationale for further clinical investigation of DIM. (aspetjournals.org)
  • Radiation therapy can be used after surgery to destroy any cancer cells that may have been left behind, which lowers the chance of recurrence. (healthline.com)
  • Chemotherapy is a systemic therapy, which means it can destroy cancer cells anywhere in the body. (healthline.com)
  • Some therapies block the production of these hormones and others interfere with the effect the hormones have on cancer cells. (healthline.com)
  • But these treatments, to some extent, easily produce side effects on normal cells, organs, and other tissues of the human body, thus accelerating the death process of cancer patients. (hindawi.com)
  • Our HCC signature covered well-established liver cancer hallmarks, and network analyses revealed coordinated interaction between several MRs. One novel MR, SEC14L2 , exerted an anti-proliferative effect in HCC cells and strongly suppressed tumor growth in a mouse model. (aging-us.com)
  • The company develops small molecule drugs that target various phases of cell cycle control for the treatment of cancer and other serious diseases. (pharmaceutical-technology.com)
  • In vitro treatment of ER-positive breast cancer cell lines with the combination of palbociclib and antiestrogens leads to increased cell senescence, which was sustained for up to 6 days following drug removal. (shu.edu)
  • Anti-estrogen therapy involves blocking the production, binding, or signaling of estrogen in cancer cells. (shu.edu)
  • Patients with triple negative breast cancer (TNBC), where the cancer cells do not express nuclear hormone receptors and human epidermal growth factor receptor 2 (HER2), have worse survival rate compared to the patients with luminal subtypes of cancer. (ku.edu)
  • Such compounds are attractive to researchers developing novel anti-cancer drugs, as conventional treatments - such as chemotherapy - are burdened by the therapy's cytotoxic effects on healthy cells. (technologynetworks.com)
  • In previous research, Kaempferia galanga L. extract - or KGE - demonstrated anti-cancer effects against Ehrlich ascites tumor cells (EATCs) in mice. (technologynetworks.com)
  • The extract was found to fragment the nucleus of the cancer cells, reducing their survival rate. (technologynetworks.com)
  • 13 Genome Plasticity and B Cell, University of Paris-Sud, Centre National de la Recherche Scientifique, Cancer Institute Gustave Roussy, Villejuif, France. (jci.org)
  • One such peptide, Lunasin , has been shown to selectively act on newly transformed cells while having no cytotoxic effect on non-tumorigenic or established cancer cell lines. (weeksmd.com)
  • Gene therapy has attracted attention for its potential to specifically and efficiently target cancer cells with minimal toxicity to normal cells. (weeksmd.com)
  • Numerous vectors have been engineered for the sole purpose of killing cancer cells, and some have successfully suppressed malignant tumours. (weeksmd.com)
  • Transcriptomic profiling of T-cell populations in non-muscle invasive and muscle invasive bladder cancer. (lu.se)
  • This is particularly true of The Journal of Cell Biology (or The Journal of Biophysical and Biochemical Cytology , as it was titled back then). (rupress.org)
  • Frontiers in cell and developmental biology. (lu.se)
  • Together, the germline and somatic mutations impair the function of proteins that regulate division and senescence, leading to uncontrolled cell growth and the formation of a melanoma. (medlineplus.gov)
  • Junctional adhesion molecule 3 (JAM3) is involved in epithelial cell junction, cell polarity, and motility. (bioone.org)
  • Next, we have shown that CCN5 protein can induce expression of estrogen receptor-α (ER-α) in mammary epithelial cells. (ku.edu)
  • In particular, ubiquitin-mediated degradation is critically important at transition points where it provides directionality and irreversibility to the cell cycle, which is essential for maintaining genome integrity. (intechopen.com)
  • Multiple endocrine neoplasia, type 4 (MEN 4) is an autosomal dominant syndrome characterized by adenomas and sometimes hyperplasia of the parathyroid glands and tumors of the pancreatic islet cells and/or pituitary gland. (msdmanuals.com)
  • When the combined expression of p27 and cyclin D1 was related to survival, patients with high levels of p27, regardless of their cyclin D1 status, did well, whilst those with low p27 had a poor outcome. (ox.ac.uk)
  • Genetic manipulations allowed analysis of changes in gene expression underlying pheromone signaling, cell cycle control, and polarized morphogenesis. (nih.gov)
  • JAM3 expression in cell-cell junctions decreased with the formation of syncytiotrophoblasts. (bioone.org)
  • Furthermore, H 2 O 2 -induced oxidative stress reduced JAM3 expression in trophoblasts and cell culture supernatants. (bioone.org)
  • Identification of PARD3 signature on PARD3 deficient H157 cell line, reconstituting the expression of PARD3 gene, with a wt and a mutant form. (nih.gov)
  • We found that mammary epithelium-specific overexpression of CCN5 in transgenic mice leads to an increase in ER-α expression and that this impact of CCN5 is not restricted to the normal cells. (ku.edu)
  • CCN5 treatment leads to an expression of functional ER-α in the TNBC cells, both in-vitro and in xenograft models, and sensitizes these cells to tamoxifen, commonly used for endocrine therapies. (ku.edu)
  • These mutations, classified as germline mutations, are typically inherited and are present in essentially all of the body's cells. (medlineplus.gov)