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

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

PROVIDER: PRJNA851072 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19754463_1.fastq.gz	Fastqsanger.gz
	SRR19754463_2.fastq.gz	Fastqsanger.gz
	SRR19754464_1.fastq.gz	Fastqsanger.gz
	SRR19754464_2.fastq.gz	Fastqsanger.gz
	SRR19754465_1.fastq.gz	Fastqsanger.gz

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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]

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

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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 [ChIP-seq]

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

| PRJNA848201 | ENA

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

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

2023-04-05 | GSE206496 | GEO

Genomic instability is an early event driving chromatin organization and “escape” from oncogene-induced senescence

Project description:Oncogene-induced senescence (OIS) is an inherent and important tumor suppressor mechanism. However, if not timely removed via immune surveillance, senescent cells will also present a detrimental side. Although this has mostly been attributed to the senescence-associated-secretory-phenotype (SASP) of these cells, we recently suggested that “escape” from the senescent state represents another unfavorable outcome. Here, we exploit genomic and functional data from a prototypical human epithelial cell model carrying an inducible CDC6 oncogene to identify an early-acquired recurrent chromosomal inversion, which harbors a locus encoding the circadian transcription factor BHLHE40. This inversion alone suffices for activation of BHLHE40 upon CDC6 induction and for driving cell cycle re-entry and malignant transformation. In summary, we provide strong evidence in support of genomic instability underlying “escape” from oncogene-induced senescence.

2021-03-31 | GSE163371 | GEO

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