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ATRX is necessary for cellular senescence and represses HRAS to drive cells from quiescence into senescence

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE74621 | GEO | 2017/09/14

SECONDARY ACCESSION(S): PRJNA301009

REPOSITORIES: GEO

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ATRX is necessary for cellular senescence and represses HRAS to drive cells from quiescence into senescence [RNA-Seq]

Project description:Senescence is a state of stable cell cycle exit that has important implications for development, physiology and disease. It is distinct from quiescence in which cells can be induced to re-enter the cell cycle. Although it is well known that there are massive changes in the heterochromatin of senescent cells, the molecular mechanisms underpinning the transition from reversible quiescence into irreversible senescence have remained elusive. Here, we demonstrate that the chromatin-remodeling enzyme ATRX is required for senescence. ATRX accumulates in nuclear foci during both replicative and cellular senescence. Using ChIP-seq and RNA-seq we identified HRAS as part of an ATRX regulated gene expression program associated with senescence. Repression of HRAS is sufficient to promote the transition of quiescent cells into senescence. Thus we conclude that the repression of HRAS is likely a direct consequence of ATRX binding and critical to how it mediates its role in senescence.

2017-09-14 | GSE74620 | GEO

ATRX is necessary for cellular senescence and represses HRAS to drive cells from quiescence into senescence [ChIP-Seq]

2017-09-14 | GSE74619 | GEO

ATRX is necessary for cellular senescence and represses HRAS to drive cells from quiescence into senescence

Project description:ATRX is necessary for cellular senescence and represses HRAS to drive cells from quiescence into senescence

| PRJNA301009 | ENA

Multileveled reduction of p21 expression by Linc-ASEN represses cellular senescence

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-09-24 | GSE128398 | GEO

Geriatric muscle stem cells switch reversible quiescence into senescence

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-12-31 | E-GEOD-53728 | biostudies-arrayexpress

Histone acetyltransferase p300 induces de novo super-enhancers to drive cellular senescence

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-02-06 | GSE105937 | GEO

MicroRNA-203 represses selection and expansion of oncogenic HRas transformed tumor initiating cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2015-07-23 | GSE66056 | GEO

Condensin-dependent chromatin condensation represses transcription globally during quiescence

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-12-27 | GSE120606 | GEO

MDM2 turnover and expression of ATRX determine the choice between quiescence and senescence in response to CDK4 inhibition.

Project description:CDK4 inhibitors (CDK4i) earned Breakthrough Therapy Designation from the FDA last year and are entering phase III clinical trials in several cancers. However, not all tumors respond favorably to these drugs. CDK4 activity is critical for progression through G1 phase and into the mitotic cell cycle. Inhibiting this kinase induces Rb-positive cells to exit the cell cycle into either a quiescent or senescent state. In this report, using well-differentiated and dedifferentiated liposarcoma (WD/DDLS) cell lines, we show that the proteolytic turnover of MDM2 is required for CDK4i-induced senescence. Failure to reduce MDM2 does not prevent CDK4i-induced withdrawal from the cell cycle but the cells remain in a reversible quiescent state. Reducing MDM2 in these cells drives them into the more stable senescent state. CDK4i-induced senescence associated with loss of MDM2 is also observed in some breast cancer, lung cancer and glioma cell lines indicating that this is not limited to WD/DDLS cells in which MDM2 is overexpressed or in cells that contain wild type p53. MDM2 turnover depends on its E3 ligase activity and expression of ATRX. Interestingly, in seven patients the changes in MDM2 expression were correlated with outcome. These insights identify MDM2 and ATRX as new regulators controlling geroconversion, the process by which quiescent cells become senescent, and this insight may be exploited to improve the activity of CDK4i in cancer therapy.

| S-EPMC4480747 | biostudies-literature

ATRX represses alternative lengthening of telomeres.

Project description:The unlimited proliferation of cancer cells requires a mechanism to prevent telomere shortening. Alternative Lengthening of Telomeres (ALT) is an homologous recombination-mediated mechanism of telomere elongation used in tumors, including osteosarcomas, soft tissue sarcoma subtypes, and glial brain tumors. Mutations in the ATRX/DAXX chromatin remodeling complex have been reported in tumors and cell lines that use the ALT mechanism, suggesting that ATRX may be an ALT repressor. We show here that knockout or knockdown of ATRX in mortal cells or immortal telomerase-positive cells is insufficient to activate ALT. Notably, however, in SV40-transformed mortal fibroblasts ATRX loss results in either a significant increase in the proportion of cell lines activating ALT (instead of telomerase) or in a significant decrease in the time prior to ALT activation. These data indicate that loss of ATRX function cooperates with one or more as-yet unidentified genetic or epigenetic alterations to activate ALT. Moreover, transient ATRX expression in ALT-positive/ATRX-negative cells represses ALT activity. These data provide the first direct, functional evidence that ATRX represses ALT.

| S-EPMC4599288 | biostudies-literature

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