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Escape From Oncogene-Induced Senescence is Controlled by POU2F2 and Memorized by Chromatin Scars

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

ORGANISM(S): Homo sapiens

PROVIDER: GSE206496 | GEO | 2023/04/05

REPOSITORIES: GEO

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Escape From Oncogene-Induced Senescence is Controlled by POU2F2 and Memorized by Chromatin Scars [Expression]

Project description:Although oncogene-induced senescence (OIS) is a potent tumor-suppressor mechanism, recent studies revealed that cells can escape from OIS with features of transformed cells. However, the mechanisms that promote OIS escape remain unclear, and evidence of post-senescent cells in human cancers is missing. Here, we unravel the regulatory mechanisms underlying OIS escape using dynamic multidimensional profiling. We demonstrate a critical role for AP1 and POU2F2 transcription factors for escape from OIS and identify ‘senescence-associated chromatin scars (SACS)’ as an epigenetic memory of OIS, detectable during colorectal cancer progression. POU2F2 levels are elevated already in precancerous lesions and as cells escape from OIS, and its expression and binding activity to cis-regulatory elements are associated with decreased patient survival. Our results support a model in which POU2F2 exploits a precoded enhancer landscape to promote senescence escape and reveal POU2F2 gene signatures and SACS as valuable biomarkers with diagnostic and prognostic potential.

2023-04-05 | GSE205692 | GEO

Escape From Oncogene-Induced Senescence is Controlled by POU2F2 and Memorized by Chromatin Scars [RNA-seq]

2023-04-05 | GSE206493 | GEO

Escape From Oncogene-Induced Senescence is Controlled by POU2F2 and Memorized by Chromatin Scars [ATAC-seq]

2023-04-05 | GSE206402 | GEO

Escape From Oncogene-Induced Senescence is Controlled by POU2F2 and Memorized by Chromatin Scars [ChIP-seq]

2023-04-05 | GSE205898 | GEO

Escape From Oncogene-Induced Senescence is Controlled by POU2F2 and Memorized by Chromatin Scars

Project description:Escape From Oncogene-Induced Senescence is Controlled by POU2F2 and Memorized by Chromatin Scars

| PRJNA851070 | ENA

Escape From Oncogene-Induced Senescence is Controlled by POU2F2 and Memorized by Chromatin Scars [Expression]

Project description:Escape From Oncogene-Induced Senescence is Controlled by POU2F2 and Memorized by Chromatin Scars [Expression]

| PRJNA847199 | ENA

Escape From Oncogene-Induced Senescence is Controlled by POU2F2 and Memorized by Chromatin Scars [ATAC-seq]

Project description:Escape From Oncogene-Induced Senescence is Controlled by POU2F2 and Memorized by Chromatin Scars [ATAC-seq]

| PRJNA850441 | ENA

Escape From Oncogene-Induced Senescence is Controlled by POU2F2 and Memorized by Chromatin Scars [RNA-seq]

Project description:Escape From Oncogene-Induced Senescence is Controlled by POU2F2 and Memorized by Chromatin Scars [RNA-seq]

| PRJNA851072 | ENA

Escape From Oncogene-Induced Senescence is Controlled by POU2F2 and Memorized by Chromatin Scars [ChIP-seq]

Project description:Escape From Oncogene-Induced Senescence is Controlled by POU2F2 and Memorized by Chromatin Scars [ChIP-seq]

| PRJNA848201 | ENA

Derepression of hTERT gene expression promotes escape from oncogene-induced cellular senescence.

Project description:Oncogene-induced senescence (OIS) is a critical tumor-suppressing mechanism that restrains cancer progression at premalignant stages, in part by causing telomere dysfunction. Currently it is unknown whether this proliferative arrest presents a stable and therefore irreversible barrier to cancer progression. Here we demonstrate that cells frequently escape OIS induced by oncogenic H-Ras and B-Raf, after a prolonged period in the senescence arrested state. Cells that had escaped senescence displayed high oncogene expression levels, retained functional DNA damage responses, and acquired chromatin changes that promoted c-Myc-dependent expression of the human telomerase reverse transcriptase gene (hTERT). Telomerase was able to resolve existing telomeric DNA damage response foci and suppressed formation of new ones that were generated as a consequence of DNA replication stress and oncogenic signals. Inhibition of MAP kinase signaling, suppressing c-Myc expression, or inhibiting telomerase activity, caused telomere dysfunction and proliferative defects in cells that had escaped senescence, whereas ectopic expression of hTERT facilitated OIS escape. In human early neoplastic skin and breast tissue, hTERT expression was detected in cells that displayed features of senescence, suggesting that reactivation of telomerase expression in senescent cells is an early event during cancer progression in humans. Together, our data demonstrate that cells arrested in OIS retain the potential to escape senescence by mechanisms that involve derepression of hTERT expression.

| S-EPMC5003242 | biostudies-literature

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