• Research into apoptosis, necrosis, autophagy, and cellular senescence is very important for understanding the intracellular functions that control cell survival and death. (dojindo.com)
  • Genes involved in cell proliferation and extracellular matrix production are down-regulated while genes promoting apoptosis are upregulated. (jcadonline.com)
  • Unlike apoptosis, senescence is a state of which cells are still alive and metabolically active. (frontiersin.org)
  • The best option would be for a cell to successfully repair any damage that occurs, but when this isn't possible (and the damage hasn't reached a critical level of inducing apoptosis) a cell will become senescent to try and avoid becoming cancerous. (sens.org)
  • Momordicine I also induced apoptosis, intracellular reactive oxygen species (ROS) production, and senescence in glioma cells. (excli.de)
  • Further, we studied the effect of HSP70-2 protein ablation on signaling cascades involved in apoptosis, cell cycle and Epithelial-Mesenchymal-Transition both in culture as well as in-vivo human breast xenograft mouse model. (biomedcentral.com)
  • Depletion of HSP70-2 in MDA-MB-231 and MCF7 cells resulted in a significant reduction in cellular growth, motility, onset of apoptosis, senescence, cell cycle arrest as well as reduction of tumor growth in the xenograft model. (biomedcentral.com)
  • In addition, we have examined the putative role of HSP70-2 in apoptosis, cell cycle arrest and epithelial-mesenchymal transition (EMT) in-vitro and in-vivo xenograft mouse model using gene silencing approach. (biomedcentral.com)
  • Compound 51 inhibited the proliferation of 13 out of 15 cancer cell lines with IC50 values between 0.27 and 6.9 muM, which correlated with the complete suppression of retinoblastoma phosphorylation and the onset of apoptosis. (proteopedia.org)
  • They can trigger apoptosis, a process of programmed cell death, when a cell becomes irreparably damaged or poses a risk of becoming cancerous. (pharmiweb.com)
  • Consistently, KLF4 depletion from breast cancer cells restores p53 levels and causes p53-dependent apoptosis. (uu.nl)
  • Curcumin modulates breast carcinogenesis through its effect on cell cycle and proliferation, apoptosis, senescence, cancer spread and angiogenesis. (natural-souls.com)
  • Results: We found that Lan C time-dependently inhibited the growth and induced apoptosis of HuCCT-1 and TFK-1 cholangiocarcinoma cells. (bvsalud.org)
  • Besides Lan C increased the reactive oxygen species (ROS) content in cholangiocarcinoma cells, decreased the mitochondrial membrane potential (MMP) and resulted in apoptosis. (bvsalud.org)
  • Senescent cells continue to survive and resist apoptosis, yet the cell cycle is arrested to prevent further proliferation [ 11 ]. (biomedcentral.com)
  • The p53 protein is an important tumor suppressor that is essential for regulating cell division, senescence, and self-destruction (apoptosis). (medlineplus.gov)
  • The senescence-associated secretory phenotype (SASP) is a hallmark of senescence with an important physiological impact, but how it is established is unclear. (rupress.org)
  • Senescent cells elicit their fibrogenic actions primarily by secreting an assortment of inflammatory and profibrotic factors known as the senescence-associated secretory phenotype (SASP). (frontiersin.org)
  • These secreted factors are collectively referred to as the senescence-associated secretory phenotype or the SASP. (sens.org)
  • Senescent cells take on a senescence associated secretory phenotype (SASP), in which production of proinflammatory cytokines, chemokines, growth factors, and proteases are increased by selective chromatin alterations [ 12 ]. (biomedcentral.com)
  • However, the accumulation of senescent cells can have detrimental consequences, such as in age-related pathologies. (rupress.org)
  • Senescent cells also undergo dramatic changes in their morphology and in the organization and architecture of their cellular compartments. (rupress.org)
  • Although senescent cells repress proliferation-promoting genes, they also induce the gene program necessary for the implementation of senescence. (rupress.org)
  • Scientists have discovered that, in the absence of resident stem cells, senescent cells can instruct neighboring somatic cells to reprogram. (dojindo.com)
  • None of the individual biomarkers that have been identified so far have been deemed to be specific to senescent cells. (dojindo.com)
  • The development of drugs that eliminate senescent cells in the body (senolytic drugs) is also attracting the attention of researchers as a possible strategy to extend healthy life expectancy. (dojindo.com)
  • Increasing evidence indicates that senescent cells could be a promising new target for therapeutic intervention known as senotherapy, which includes depleting senescent cells, modulating SASP and restoration of senescence inhibitors. (frontiersin.org)
  • We also highlight potential options of targeting senescent cells for the treatment of CKD. (frontiersin.org)
  • We also highlight potential options for targeting senescent cells in developing therapeutics for CKD patients. (frontiersin.org)
  • Researchers have found that senescent cells accumulate in our body as we age. (sens.org)
  • As the interest in defining senescent cells has grown, so has the interest in deciphering why they exist in the first place. (sens.org)
  • The leading hypothesis for why senescent cells exist is that they serve as a preventative measure against cancer. (sens.org)
  • Because they are no longer dividing, it might sound like senescent cells are inactive and prevent cancer by completely shutting down. (sens.org)
  • In reality, senescent cells are highly metabolically active which means that there are still many cellular processes happening within the cytoplasm. (sens.org)
  • Senescent cells secrete various proteins and molecules that cause inflammation. (sens.org)
  • Senescent cells are great for the initial prevention of cancer, but remember the SASP I just mentioned? (sens.org)
  • Although senescent cells start out as helpers that prevent cancer, too many of them can become a detriment to human health. (sens.org)
  • Researchers have found that senescent cells accumulate around the body as we age, so conditions such as Alzheimer's disease, heart disease, and liver fibrosis may be significantly worsened by the increased inflammation that comes with the accumulation of senescent cells. (sens.org)
  • There is still a lot to be discovered about how senescent cells work and scientists are very interested in understanding what other roles they might be playing in a wide variety of diseases. (sens.org)
  • This has also prompted many research groups to investigate how we might be able to remove senescent cells around the body with drugs or cell therapies which could help improve the health of many individuals. (sens.org)
  • Because age-related cellular senescence and type 2 diabetes (T2D) have been recognised as risk factors for CRC development, the recent finding that type 2 diabetic patients present an elevated circulating volume of senescent cells raises the question whether type 2 diabetes facilitates the process of CRC tumorigenesis by inducing premature cell senescence. (frontiersin.org)
  • Over lifetime, due to the action of several stressors such as DNA damage and telomere shortening, senescent cells accumulate in the organism and release a variety of pro-inflammatory cytokines responsible for low-grade inflammation. (frontiersin.org)
  • Senescent ERas cells do not develop cytoprotective autophagy upon inhibition of MEK/ERK pathway due to spatial dissociation of lysosomes and autophagosomes in the senescent cells. (aging-us.com)
  • Senescent cells are unable to form the autophagolysosomes and to remove the damaged mitochondria resulting in apoptotic death. (aging-us.com)
  • Our data show that suppression of MEK/ERK pathway in senescent cells provides a new strategy for elimination of Ras-expressing cells. (aging-us.com)
  • A team led by Professor Lorna Harries, Professor of Molecular Genetics at the University of Exeter, has discovered a new way to rejuvenate inactive senescent cells. (neurosciencenews.com)
  • The University of Exeter research team, working with Professor Richard Faragher and Dr Elizabeth Ostler from the University of Brighton, found that splicing factors can be switched back on with chemicals, making senescent cells not only look physically younger, but start to behave more like young cells and start dividing. (neurosciencenews.com)
  • As we age, our tissues accumulate senescent cells which are alive but do not grow or function as they should. (neurosciencenews.com)
  • Senescent cells, which can be found in most organs from older people, also have fewer splicing factors. (neurosciencenews.com)
  • Although cellular senescence plays an important role in tissue homeostasis, the dramatic accumulation of senescent cells in old age has deleterious effects on damage repair and systemic inflammation [ 11 ]. (biomedcentral.com)
  • Boosting your mitochondria, and improving the clearing and recycling of these senescent cells are among the most effective strategies that I have seen clinically for combating aging and improving your general health. (drjohnlieurance.com)
  • Cellular senescence refers to active cells that eventually enter a state of irreversible growth arrest. (hindawi.com)
  • It was also shown that inhibition of the p16 tumour suppressor gene delays growth arrest and therefore senescence of MSC [ 16 ]. (hindawi.com)
  • We also assessed the effect of WSC on the expression of genes involved in cell cycle arrest and inflammation. (nih.gov)
  • However, WSC induced cell cycle arrest and cellular senescence mediated by the p53-p21 pathway. (nih.gov)
  • Cellular senescence was first identified as a type of irreversible cell cycle arrest that occurs when cells reach the end of their replicative potential ( Hayflick and Moorhead, 1961 ). (rupress.org)
  • The defining characteristic of senescence is a highly stable cell cycle arrest, triggered by the up-regulation of cyclin-dependent kinase inhibitors such as p16 INK4a and p21 CIP1a . (rupress.org)
  • Genes necessary for cell cycle progression, such as E2F-dependent genes, are incorporated into the SAHF and are thereby silenced, contributing to the stability of the growth arrest. (rupress.org)
  • Selumetinib causes long-term G1 arrest accompanied by reduced expression of DNA replication and repair genes, but cells stochastically re-enter the cell cycle during treatment despite continued repression of pERK1/2. (babraham.ac.uk)
  • Combined treatment with selumetinib and a dose of palbociclib sufficient to reinforce G1 arrest in selumetinib-sensitive cells, but not to impair proliferation of resistant cells, delays the emergence of resistant colonies, meaning that escape from G1 arrest is critical in the formation of resistant clones. (babraham.ac.uk)
  • Irreversible cell cycle arrest is one of the phenomena that characterize cellular senescence. (dojindo.com)
  • Doxorubicin (DOX) is known as an anticancer drug that acts in the G2/M phase of the cell cycle to arrest cell proliferation and induce cellular senescence (see the upper left figure). (dojindo.com)
  • Aging kidney and CKD share many common characteristic features with increased cellular senescence, a conserved program characterized by an irreversible cell cycle arrest with altered transcriptome and secretome. (frontiersin.org)
  • Cellular senescence is characterized by an irreversible and permanent cell cycle arrest coupled with altered transcriptome and secretome. (frontiersin.org)
  • Instead of devolving into unchecked proliferation, it undergoes a permanent arrest of the cell cycle which could prevent cancers from growing rapidly. (sens.org)
  • Senescence is a stress-response cellular state characterised by proliferative arrest but active metabolism ( 7 ). (frontiersin.org)
  • In addition, SNHG4 or RRM2 knockdown significantly induced cell cycle arrest and cell senescence, and inhibited DNA damage repair and cell proliferation, and the effects can be partially reversed by let-7a knockdown or RRM2 reoverexpression. (biomedcentral.com)
  • AKI603 inhibited cell proliferation and colony formation capacities in imatinib-resistant CML cells by inducing cell cycle arrest with polyploidy accumulation. (scite.ai)
  • According to recent data, Ras-transformed cells require autophagy to survive and maintain malignant phenotype [ 5 - 10 ]. (aging-us.com)
  • Since then, many research teams have become interested in determining the hallmarks of cell senescence, the factors that induce it, and the effect of senescence on other cells and the body as a whole. (sens.org)
  • Age-related and metabolic diseases such as type 2 diabetes (T2D) represent a source of cellular stress due to their disruptive effect on normal physiological processes and, therefore, can induce premature senescence ( 10 ). (frontiersin.org)
  • Hence, it is of great importance to investigate the mechanisms that induce enzalutamide resistance in prostate cancer cells. (biomedcentral.com)
  • Further, PARP-1 and PARP-1 fragment's involvement in various forms of cell death e.g. autophagy, necrosis and parthanatos are also indicated. (shu.edu)
  • Macroautophagy (hereafter referred to as autophagy) plays an important role in cancer cells survival upon various conditions of intra- and extracellular stress. (aging-us.com)
  • Despite a large number of promising inhibitors for Ras/Raf/MEK/ERK pathway, recent works show that cancer cells often develop an autophagy-dependent resistance to inhibitors of Ras pathway [ 16 ]. (aging-us.com)
  • Given that autophagy is initiated upon suppressed mTORC1 activity, a protective autophagy in Ras-transformed cells with a high level of mTORC1 activity appears to be mTORC1-independent [ 20 , 21 ]. (aging-us.com)
  • One of the mechanisms of high basal autophagy activity in cancer Ras-expressing cells might be associated with high PP2A phosphatase activity targeting directly ULK1-Ser757 that could explain apparent contradiction: maintenance of high mTORC1 functions and high autophagic activity simultaneously [ 22 ]. (aging-us.com)
  • We will dig into a few technical subjects such as NAD+, Autophagy, Mitophagy, and Cellular Senescence, Microbiome Swarming and Stem Cell Survival to understand why this protocol can be maximized to achieve a much stronger healing effect. (drjohnlieurance.com)
  • We demonstrate that PLL provides favourable microenvironment for MSC culture by reversing the replicative senescence. (hindawi.com)
  • Unlike embryonic stem cells, adult stem cells (MSCs) have a limited lifespan and stop proliferating during in vitro culture due to replicative senescence [ 8 ]. (hindawi.com)
  • Moreover, replicative senescence of MSCs exhibits reduced functionality, and cellular senescence might impair the regenerative potential of MSCs [ 10 ]. (hindawi.com)
  • Studies show that replicative senescence or cellular senescence is induced by intrinsic or extrinsic environmental factors [ 11 ]. (hindawi.com)
  • In this review, we will discuss the mechanisms according to which T2D induces cellular senescence and the role of type 2 diabetes-induced cellular senescence in the pathogenesis and progression of colorectal cancer. (frontiersin.org)
  • In addition, their osteogenic differentiation potential was increased, and genes involved in cell adhesion, FGF-2 signalling, cell cycle, stemness, cell differentiation, and cell proliferation were upregulated, compared to that of the MSCs cultured on uncoated plates. (hindawi.com)
  • Deletions of multiple GID subunits compromise cell proliferation, and this defect is accompanied by deregulation of critical cell cycle markers such as the retinoblastoma (Rb) tumor suppressor, phospho-Histone H3 and Cyclin A. We identify the negative regulator of pro-proliferative genes Hbp1 as a bonafide GID/CTLH proteolytic substrate. (elifesciences.org)
  • In addition, Kevetrin increased expression of p53 target genes such as p21 (Waf1), an inhibitor of cell cycle progression. (shu.edu)
  • While there are ongoing research projects to define new markers or causes of senescence, we do know that senescence can be induced by damage to DNA, shortening of telomeres (which are the protective caps at the end of DNA molecules), mitochondrial damage, and something called epigenetic factors, which refers to changes to our chromosomes that affect the way DNA is packaged and genes are expressed. (sens.org)
  • Our data suggests that using chemicals to switch back on the major class of genes that are switched off as we age might provide a means to restore function to old cells. (neurosciencenews.com)
  • These old cells lose the ability to correctly regulate the output of their genes. (neurosciencenews.com)
  • When activated, genes make a message that gives the instructions for the cell to behave in a certain way. (neurosciencenews.com)
  • Most genes can make more than one message, which determines how the cell acts. (neurosciencenews.com)
  • Tumor suppressor genes code for proteins that inhibit cell division and growth, acting as a control mechanism to prevent excessive cell proliferation. (pharmiweb.com)
  • Tumor suppressor genes can promote cellular senescence, a state in which cells stop dividing, preventing the replication of damaged DNA. (pharmiweb.com)
  • We describe the identification of KLF4 in a functional genomic screen for genes that bypass RASV12-induced senescence. (uu.nl)
  • The function of differentially expressed E2Fs and their neighboring genes were mainly linked to P53 signaling pathway, cell cycle, and oocyte meiosis. (fortunepublish.com)
  • Prior to senescence, mutant RasV12 activation in primary human fibroblasts compromised mitosis, associated with abnormal expression of mitotic genes that enter M-phase. (nih.gov)
  • Somatic mutations in other genes involved in cell growth are also needed for a melanoma to develop. (medlineplus.gov)
  • Finally, we demonstrate that Polycomb proteins and associated epigenetic marks are crucial for the control of the replication timing of the INK4a/ARF locus during senescence. (plos.org)
  • Our results suggest that in young cells Polycomb proteins are recruited to the INK4/ARF locus through CDC6 and the resulting silent locus is replicated during late S-phase. (plos.org)
  • Evidence supporting the direct control of the cell cycle by Pc-G proteins in vertebrates came from studies on mouse Bmi1 mutants. (plos.org)
  • Cellular proteostasis involves the coordinated and compensatory action of pathways that control biogenesis, folding, trafficking and breakdown of proteins allowing the cell to adapt to physiological or pathological environmental changes. (elifesciences.org)
  • The activation/upregulation of these proteins are used as indicators of cellular senescence. (dojindo.com)
  • These marker proteins are known to be tumor suppressors and regulate the cell cycle mainly through two pathways (p16Ink4a-RB and p53-p21CIP1). (dojindo.com)
  • Well, it turns out that some of those inflammatory proteins and molecules that make up the SASP can have negative effects on other cells and tissues. (sens.org)
  • Some tumor suppressor proteins are involved in maintaining cell adhesion, preventing cells from breaking away and spreading to other parts of the body (metastasis). (pharmiweb.com)
  • Cell adhesion molecules are a diverse group of proteins that play a crucial role in mediating cell-to-cell interactions and cell-to-extracellular matrix interactions. (pharmiweb.com)
  • The proper development and homeostasis of tissues and organs at the cellular level are ensured by a finely and timely regulated progression of the cell division cycle, which requires the perfectly harmonized activity of numerous protein kinases/phosphatases and regulatory proteins. (mdpi.com)
  • Both proteins are also involved in stopping cell division in older cells (senescence). (medlineplus.gov)
  • These proteins help regulate the cell cycle, which is the cell's way of replicating itself in an organized, step-by-step fashion. (medlineplus.gov)
  • The p14(ARF) and p53 proteins are often made in cells that are unable to undergo cell division. (medlineplus.gov)
  • 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)
  • 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)
  • This miRNA functions as a tumor suppressor and dysregulation or loss of the host gene from which this miRNA is processed is associated with cancer progression in numerous cell types. (cancerindex.org)
  • As a result, changes in SA-ß-Gal expression, cell cycle progression, and mitochondrial membrane potential were observed. (dojindo.com)
  • Common detection indicators for assessing cellular senescence include features related to cell cycle progression (DNA synthesis, p16/p21 expression, etc.), features related to morphology (of the cell, nucleus, nucleolus, etc. (dojindo.com)
  • While developmental senescence and acute senescence may positively contribute to the fine-tuning of embryogenesis and injury repair, chronic senescence, when unresolved promptly, plays a crucial role in kidney fibrogenesis and CKD progression. (frontiersin.org)
  • We have reported that the expression of BMI1 , a member of PcG, in hematopoietic stem cells or progenitor cells predicts the prognosis of patients with MDS and progression to acute leukemia. (karger.com)
  • Cyclin-dependent kinases (CDKs) are serine/threonine protein kinases that act as key regulatory elements in cell cycle progression. (proteopedia.org)
  • Many ORs are expressed by tumor cells and tissues, suggesting that they may be associated with cancer progression or may be cancer biomarkers. (bmbreports.org)
  • However, binding of p16(INK4A) blocks CDK4's or CDK6's ability to stimulate cell cycle progression. (medlineplus.gov)
  • Cellular senescence, which is morphologically characterized by an enlarged and flattened cell shape, was first described by Hayflick [ 9 ]. (hindawi.com)
  • Cellular senescence was reported by Hayflick in 1981. (dojindo.com)
  • The concept of senescence was first discovered in the 1960's by two scientists named Leonard Hayflick and Paul Moorhead. (sens.org)
  • In the absence of Bmi1, M33, or Phc2, primary embryonic fibroblasts (MEFs) are unable to progress into S phase, undergo premature senescence after only a few passages in culture and show an increased accumulation of the tumor suppressors p16 INK4a , p19 ARF and p15 INK4b [4] , [10] . (plos.org)
  • Recently, various fields have given particular attention to cellular senescence due to the recent discoveries of SASP (a known cancer-causing factor) and senescence-related phenomena in stem cell research. (dojindo.com)
  • Nephron progenitors, the self-renewing cells that give rise to nephrons, are particularly metabolically active, relying primarily on glycolysis for energy generation early in development. (lww.com)
  • Nephron progenitors, the cell population that give rise to the functional unit of the kidney, are metabolically active and self-renew under glycolytic conditions. (lww.com)
  • In addition cellular senescence constitutes a tumor suppressor mechanism [1] , [2] . (plos.org)
  • In this review, we discuss current understanding of the role and mechanism of cellular senescence in kidney fibrosis. (frontiersin.org)
  • In this review, we summarize the evidence linking cellular senescence to the pathogenesis of CKD and discuss current understanding of the mechanism and regulators controlling senescence. (frontiersin.org)
  • So far, it seems like cellular senescence is a great mechanism to have in our bodies, but as is the case with many cellular processes, too much of a good thing can become a bad thing. (sens.org)
  • Recently, evidence has been accumulating on the molecular mechanism underlying self-renewal of stem cells. (karger.com)
  • By using a direct in vivo shRNA screen, we show that liver cancer cells that have mutations in the gene encoding the tumor suppressor protein p53 (Trp53 in mice and TP53 in humans) and that are driven by the oncoprotein NRAS become addicted to MYC stabilization via a mechanism mediated by aurora kinase A (AURKA). (scite.ai)
  • We explored the potential mechanism underlying the anticancer activity of Lan C on cholangiocarcinoma cells by flow cytometry, western blot, immunofluorescence, transcriptomics sequencing, network pharmacology and in vivo experiments. (bvsalud.org)
  • Oncogene-induced senescence (OIS) is a tumor suppression mechanism that blocks cell proliferation in response to oncogenic signalling. (nih.gov)
  • Plasmid driven short hairpin RNA approach was employed to validate the role of HSP70-2 in cellular proliferation, senescence, migration, invasion and tumor growth. (biomedcentral.com)
  • Crucial role in orchestrating a fine balance between cellular proliferation, cell death, and DNA repair in human embryonic stem cells (hESCs). (proteopedia.org)
  • Use Vitronectin XF™ with mTeSR™1 , mTeSR™ Plus , TeSR™-E8™ , or TeSR™-AOF medium to provide a defined culture system for the maintenance of human embryonic stem (ES) cells and human induced pluripotent stem (iPS) cells under feeder-free conditions. (stemcell.com)
  • 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)
  • Agherbi H, Gaussmann-Wenger A, Verthuy C, Chasson L, Serrano M, Djabali M (2009) Polycomb Mediated Epigenetic Silencing and Replication Timing at the INK4a/ARF Locus during Senescence. (plos.org)
  • The tumor suppressor pathways, ARF/MDM2/p53 and p16 INK4a /Rb, have been shown to play critical roles in the induction of cellular senescence [3] . (plos.org)
  • Bruggeman SWM, Valk-Lingbeek ME, van der Stoop PPM, Jacobs JJL, Kieboom K, et al: Ink4A and Arf differentially affect cell proliferation and neural stem cell self-renewal in Bmi1-deficient mice. (karger.com)
  • In this way, p16(INK4A) controls 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)
  • By embryonic day 15.5, kidneys of nephron progenitor cell-specific VHL knockout mice begin to exhibit reduced maturation of nephron progenitors. (lww.com)
  • The mudpuppy is an aquatic salamander commonly used by embryologists because its large embryonic cells and nuclei are easy to see. (asu.edu)
  • Platt followed the paths of cells in developing mudpuppy embryos to see how embryonic cells migrated during the formation of the head. (asu.edu)
  • Boyer LA, Plath K, Zeitlinger J, Brambrink T, Medeiros LA, et al: Polycomb complexes repress developmental regulators in murine embryonic stem cells. (karger.com)
  • These molecules are essential for embryonic development, wound healing, immune cell recognition, and many other physiological functions. (pharmiweb.com)
  • Androgen deprivation-induced senescence (or ADIS) refers to the induction of cellular senescence as a result of androgen deprivation therapy. (wikipedia.org)
  • The induction and control mechanisms of cellular senescence - in which genetic and external factors are intricately involved - have yet to be fully elucidated. (dojindo.com)
  • The extracellular matrix (ECM) provides structural and biochemical support to the surrounding cells, and it has been used as a coating substrate for cell culture. (hindawi.com)
  • The molecules are found on the cell surface, where they facilitate adhesion to neighboring cells or the extracellular matrix, creating stable cell structures and supporting tissue organization. (pharmiweb.com)
  • However, MSCs need to be expanded in vitro in order to obtain sufficient cells for clinical trials since they are extremely rare in various tissues. (hindawi.com)
  • It is hard to preserve the important characteristics such as proliferation capacity and stemness of MSCs the inadequate cultivating microenvironment in vitro . (hindawi.com)
  • In this manuscript, we report the in vitro mutagenicity of waterpipe smoke condensate (WSC), the alteration in cellular parameters of lung alveolar cells in response to WSC exposure and discuss the implication of cellular responses in the pathophysiology of chronic obstructive pulmonary disease (COPD). (nih.gov)
  • Indeed, Hbp1 accumulates in cells lacking GID/CTLH activity, and Hbp1 physically interacts and is ubiquitinated in vitro by reconstituted GID/CTLH complexes. (elifesciences.org)
  • In vitro and in vivo experiments showed that SNHG4 overexpression markedly enhanced cell resistance to enzalutamide. (biomedcentral.com)
  • Tumor immunohistochemistry showed that nude mice transplanted with human cholangiocarcinoma cells treated with Lan C exhibited decreased STAT3 expression and increased caspase-9 and caspase-3 expression in tumors, consistent with the in vitro results. (bvsalud.org)
  • Here, we developed CellAgeClock, a new epigenetic clock that measures subtle ageing changes in primary human cells in vitro . (biorxiv.org)
  • Our method expands the scope of CpG methylation profiling from measuring human chronological and biological age from human samples in years, to accurately and rapidly detecting anti-ageing potential of drugs using human cells in vitro , providing a novel accelerated discovery platform to test sought after geroprotectors. (biorxiv.org)
  • An image depicting head and neck squamous cell carcinoma in vitro can be seen below. (medscape.com)
  • Head and neck squamous cell carcinoma in vitro (cell culture). (medscape.com)
  • Importantly, mitotic slippage and oncogene signalling synergistically induced senescence and key senescence regulators p21 and p16. (nih.gov)
  • This observation prompted us to characterise the cell-autonomous cytotoxic and anti-proliferative profile of gomesin in DFTD cells and in comparison, to non-transformed (healthy) Tasmanian devil fibroblasts (FIBS). (nature.com)
  • It was discovered when pulmonary fibroblasts slowed down their proliferation and eventually ended in cell death after cell passaging had been performed for more than 8 months. (dojindo.com)
  • We studied whether cellular senescence induced by HDAC inhibitor sodium butyrate in E1a+cHa-Ras -transformed rat embryo fibroblasts (ERas) and A549 human Ki-Ras mutated lung adenocarcinoma cells would enhance the tumor suppressor effect of MEK/ERK inhibition. (aging-us.com)
  • Cancer Lett, 300:215-224.doi:10.1016/j. squamous cell carcinoma in north-eastern Iran. (who.int)
  • The mechanisms underlying the cellular senescence of MSCs are still poorly understood. (hindawi.com)
  • Cellular senescence is a complex process, and its molecular mechanisms are unknown. (hindawi.com)
  • A switch from glycolysis to mitochondrial respiration drives these cells toward differentiation, but the mechanisms that control this switch are poorly defined. (lww.com)
  • Cancer cells exploit a variety of protective mechanisms that allow them to acquire selective advantage and proliferate under unfavorable conditions. (aging-us.com)
  • The chemotherapeutics employed in curative and palliative regimens in many cases preclude cell division via a variety of mechanisms. (mhmedical.com)
  • In different immune cell types, each MiT family member is shown to play distinct or redundant roles and we expect that there is far more to learn about their functions and regulatory mechanisms in host defense and inflammatory responses. (molcells.org)
  • [ 6 ] These events lead the cancer cell to escape normal cell growth and control mechanisms, to avoid system control mechanisms (ie, immunologic surveillance), and to establish a nutrient supply. (medscape.com)
  • The differentiation of mesenchymal stem cells (MSCs) into multiple cell lineages can be exploited as an attractive strategy for cell-based therapy and regenerative medicine [ 1 ]. (hindawi.com)
  • The ECM provides structural and biochemical support to the cells and has various other functions including cell adhesion, cell to cell communication, and differentiation [ 17 , 18 ]. (hindawi.com)
  • Neuronal differentiation and cell-cycle programs mediate response to BET-bromodomain inhibition in MYC-driven medulloblastoma. (cancerindex.org)
  • Support the growth and differentiation of human pluripotent stem cells by using Vitronectin XF™, a defined and xeno-free cell culture matrix. (stemcell.com)
  • AKAP12 knockdown in benign meningioma cells SF4433 increases proliferation, cell cycle, migration, invasion, and confers an anaplastic profile. (nature.com)
  • We also report that HSP70-2 plays an important role in cellular growth, migration and invasion of breast cancer cells and tumor growth of breast cancer xenograft. (biomedcentral.com)
  • L1CAM plays a role in neural development, axon guidance, and cell migration. (pharmiweb.com)
  • Our findings demonstrate that acquisition of MEK inhibitor resistance often occurs through gene amplification and can be suppressed by impeding cell cycle entry in drug. (babraham.ac.uk)
  • Among them, cyclin-dependent kinases (CDK)s with their modulatory partners, cyclins, represent the major players acting with switch-like behavior to turn on cell growth, through the control of chromatin replication and condensation, gene transcription, assembly of the mitotic spindle, and proper cytodieresis. (mdpi.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)
  • More recently, cellular senescence has been considered as an additional cause of age-related tumorigenesis. (frontiersin.org)
  • This is the multihit theory of tumorigenesis, in which a series of multiple triggering events in the genetic and cellular makeup of a cell ultimately cause cancer. (medscape.com)
  • Remarkably, inactivation of the cyclin-D1 target and the cell-cycle inhibitor p21CIP1 not only neutralizes the cytostatic action of KLF4, but also collaborates with KLF4 in oncogenic transformation. (uu.nl)
  • ERKi treatment of cells drives the poly-ubiquitylation and proteasome-dependent turnover of ERK2 and pharmacological or genetic inhibition of Cullin-RING E3 ligases prevents this. (babraham.ac.uk)
  • Surprisingly, inhibition of AurA by AKI603 induced leukemia cell senescence in both BCR-ABL wild type and T315I mutation cells. (scite.ai)
  • CDK4 and CDK6 normally stimulate the cell to continue through the cycle and divide. (medlineplus.gov)
  • KLRG1 inhibits cell activation and proliferation, and is a marker of T cell senescence. (biolegend.com)
  • Inhibits cell activation and proliferation, marker of T cell senescence. (biolegend.com)
  • However, in earlier studies, clonal analysis was restricted by the lack of a cell marker, present at all times, that makes a distinction between the two parental cell types in situ. (asu.edu)
  • In addition, we designed and screened a panel of gomesin analogues with amino acid modifications that were predicted to influence cell viability. (nature.com)
  • We tested four major extracts of M. charantia and found that momordicine I reduced glioma cell viability without serious cytotoxic effects on astrocytes. (excli.de)
  • Several Ig-superfamily CADMs are crucial for immune cell interactions. (pharmiweb.com)
  • Mesenchymal stem cells (MSCs) possess great therapeutic potential. (hindawi.com)
  • Lastly, we will explore the current therapeutic approaches and challenges in targeting senescence. (frontiersin.org)
  • Our results indicate that the cytotoxic effect of momordicine I on glioma cells suggests its potential therapeutic application to GBM treatment. (excli.de)
  • With this background information as a foundation, we then discuss each of the key questions in relation to the upcoming therapeutic trial and critically assess if the time is ripe for clinical translation of parthenogenetic stem cell technology in Parkinson's disease. (lu.se)
  • Cells are potent to go under abnormal growth processes and finally lead to tumor/cancer. (pharmiweb.com)
  • However, in untransformed cells, KLF4 acts as a potent inhibitor of proliferation. (uu.nl)
  • To study the potential role in this metabolic shift of von Hippel-Lindau (VHL), a protein component of a ubiquitin ligase complex, the authors generated nephron progenitor cell-specific VHL knockout mice. (lww.com)
  • The foamy stromal cells between the capillaries stain positive for glial fibrillary acid protein and neuron-specific enolase. (medscape.com)