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Links from GEO DataSets

Items: 20

1.

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

(Submitter supplied) 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. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL17586
34 Samples
Download data: CEL
Series
Accession:
GSE205692
ID:
200205692
2.

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

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by array; Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platforms:
GPL16791 GPL24676 GPL17586
101 Samples
Download data: BW, CEL, NARROWPEAK
Series
Accession:
GSE206496
ID:
200206496
3.

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

(Submitter supplied) 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. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
12 Samples
Download data: BW, TXT
Series
Accession:
GSE206493
ID:
200206493
4.

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

(Submitter supplied) 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. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
25 Samples
Download data: BW, NARROWPEAK
Series
Accession:
GSE206402
ID:
200206402
5.

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

(Submitter supplied) 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. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
30 Samples
Download data: BW, NARROWPEAK
Series
Accession:
GSE205898
ID:
200205898
6.

Functional CRISPR Screen Identifies AP1-associated Enhancer regulating FOXF1 to modulate Oncogene-Induced Senescence

(Submitter supplied) We carried out CRISPR-Cas9 functional screen focused on AP-1 bound enhancers that are activated upon oncogenic stress. The screen discovered Enh.AP1.OIS1 - an enhancer bound by AP1 that is required for activation of oncogene-induced senescence (OIS) response. We applied RNA-seq analysis to RASG12V-activated BJ cells transduced with either sgRNAs targeting AP-1 bound enhancer (sgRNA-69 or sgRNA71), or sgRNA targeting the target gene FOXF1 or non-targeting control sgRNA (sgNT)
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
4 Samples
Download data: TXT
7.

Massive reshaping of genome - nuclear lamina interactions during oncogene induced senescence (genome tiling)

(Submitter supplied) Background. Cellular senescence is a mechanism that virtually irreversibly suppresses the proliferative capacity of cells in response to various stress signals. This includes the expression of activated oncogenes, which cause Oncogene-Induced Senescence (OIS). A body of evidence points to the involvement of chromatin reorganization, including the formation of senescence-associated heterochromatic foci (SAHF). more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by genome tiling array
Platform:
GPL10559
1 Sample
Download data: PAIR
Series
Accession:
GSE76646
ID:
200076646
8.

Massive reshaping of genome - nuclear lamina interactions during oncogene induced senescence

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing; Genome binding/occupancy profiling by genome tiling array
Platforms:
GPL11154 GPL10559
37 Samples
Download data: PAIR
Series
Accession:
GSE76605
ID:
200076605
9.

Massive reshaping of genome - nuclear lamina interactions during oncogene induced senescence (DamID-seq)

(Submitter supplied) Background. Cellular senescence is a mechanism that virtually irreversibly suppresses the proliferative capacity of cells in response to various stress signals. This includes the expression of activated oncogenes, which cause Oncogene-Induced Senescence (OIS). A body of evidence points to the involvement of chromatin reorganization, including the formation of senescence-associated heterochromatic foci (SAHF). more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
12 Samples
Download data: CSV, TXT
Series
Accession:
GSE76594
ID:
200076594
10.

Massive reshaping of genome - nuclear lamina interactions during oncogene induced senescence (RNA-seq)

(Submitter supplied) Cellular senescence is a mechanism that virtually irreversibly suppresses the proliferative capacity of cells in response to various stress signals. This includes the expression of activated oncogenes, which cause Oncogene-Induced Senescence (OIS). A body of evidence points to the involvement of chromatin reorganization, including the formation of senescence-associated heterochromatic foci (SAHF). The nuclear lamina (NL) is an important contributor to genome organization and has been involved in cellular senescence and organismal aging. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
24 Samples
Download data: TXT
Series
Accession:
GSE75643
ID:
200075643
11.

HDAC4 controls senescence and aging by safeguarding the epigenetic identity and  ensuring the genomic integrity

(Submitter supplied) Purpose: Define HDAC4 signature Outcome: HDAC4 is required for the repression of a senescence signature. HDAC4 KO promotes the expression of inflammatory genes, the derepression of ERVs and the accumulation of DNA damage. All together these signalling pathways lead to permanent cell-cycle arrest in low grade tumor cells and pre-transformation models, while they weaken the replicative potential of primary normal cells.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10558
12 Samples
Download data: TXT
Series
Accession:
GSE150427
ID:
200150427
12.

HDAC4 controls senescence and aging by safeguarding the epigenetic identity and  ensuring the genomic integrity

(Submitter supplied) Purpose: Define the epigenetic program of HDAC4 Outcome: HDAC4 controls the H3K27me3 of repetitive elements of retroviral origin (ERVs) and the H3K27 deacetylation of typical and super-enhancers found to be activated during senescence. The former response is due to the remodeling of the chromatin that sorrounds ERVs, while the latter is directly mediated by HDAC4 binding to the chromatin and the local deacetylation.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
7 Samples
Download data: BW
Series
Accession:
GSE149644
ID:
200149644
13.

DNMT1 drives 4D genome rewiring during oncogene induced senescence

(Submitter supplied) While, transcriptional and epigenetic changes associated senescence processes are well studied, the 3D chromatin changes associated with it remains elusive. In this study, we have generated genome wide chromatin interaction maps (Hi-C), epigenetic (ChIP-Seq), replication-timing and gene expression (RNA-Seq) profiles from replication induced (RS) and oncogene induced (OIS) senescent cells. As senescence associated heterochromatin foci (SAHFs) differentiates both RS and OIS nuclei, we identified the regions that constitute SAHFs and called them Senescence Associated Heterochromatin Domains (SAHDs). more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing; Other; Methylation profiling by high throughput sequencing
Platform:
GPL11154
92 Samples
Download data: BED, BW, TAR, TXT
14.

The SCN9A channel and plasma membrane depolarization promote cellular senescence through Rb pathway

(Submitter supplied) Oncogenic signals can induce premature senescence (OIS) in normal human cells causing a proliferation arrest and the elimination of these defective cells by immune cells. In order to identify new regulators of OIS, we performed a loss-of-function genetic screen and identified that the loss of SCN9A sodium channel allowed cells to escape from OIS. Here we studied the transcriptome profiles of an OIS model based on human mammary epithelial cells stably expressing hTert to be immortalized and MEK:ER, a 4-hydroxytamoxifen (4-OHT) inducible oncogene MEK:ER (HEC-TM cells), to induce the oncogenic signal. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL13497
15 Samples
Download data: TXT
Series
Accession:
GSE110884
ID:
200110884
15.

Mapping H4K20me3 onto the chromatin landscape of senescent cells indicates a function in control of cell senescence and tumor suppression through preservation of genetic and epigenetic stability.

(Submitter supplied) Histone modification H4K20me3 and its methyltransferase SUV420H2 have been implicated in suppression of tumorigenesis. The underlying mechanism is unclear, although abundance of H4K20me3 increases during cellular senescence. Cellular senescence is a stable proliferation arrest and tumor suppressor process, triggered by diverse molecular cues, including activated oncogenes. Here, we set out to better understand the function of H4K20me3 in senescence and tumor suppression.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
8 Samples
Download data: BED
Series
Accession:
GSE81969
ID:
200081969
16.

Genome-wide mapping of H4K20me3 in proliferating and senescent IMR90 cells.

(Submitter supplied) Cellular senescence is a stable proliferation arrest and tumor suppressor mechanism. Abundance of histone modification, H4K20me3, has been reported to increase in senescent cells. Generally, H4K20me3 promotes formation of compacted transcriptionally silent constitutive heterochromatin, but its specific role in senescence is unknown. Here, we show that in senescent cells H4K20me3 is enriched at specific families of gene repeats (ZNFs, Olfactory Receptors, Protocadherins), and DNA sequences contained within senescence-associated heterochromatin (senescence-associated heterochromatin (SAHF)). more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL10999
4 Samples
Download data: BED
Series
Accession:
GSE59316
ID:
200059316
17.

Histone chaperone HIRA orchestrates H4K16ac-decorated dynamic chromatin in senescent cells and is required for suppression of oncogene-induced neoplasia.

(Submitter supplied) Cellular senescence is a stable proliferation arrest that suppresses tumorigenesis. Histone chaperone HIRA deposits nucleosome-destabilizing histone variant H3.3 into chromatin in a DNA replication-independent manner. Histone H3.3 and a subset of other typically “replication-dependent” core histones were expressed in non-proliferating senescent cells, the latter linked to alternative mRNA splicing and polyadenylation. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL10999
22 Samples
Download data: BED, BIGWIG, CSV
Series
Accession:
GSE56307
ID:
200056307
18.

Expression data from PD32 and PD88 IMR90

(Submitter supplied) IMR90 cells were passaged until replicative senescence and compared with proliferating cells.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL10999
4 Samples
Download data: BIGWIG
Series
Accession:
GSE53356
ID:
200053356
19.

Expression data from ER32 and ER32.40HT IMR90

(Submitter supplied) IMR90 cells were infected with pLNC-RAS:ER (from Jesus Gil lab) with retroviral gene transfer. Infected cells were drug selected G418. The cells were induced either with ethanol as control or with 100nM final conc 4-hydroxytamoxifen (sigma H7904) for ectopic expression of protein
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL10999
4 Samples
Download data: BIGWIG
Series
Accession:
GSE52848
ID:
200052848
20.

Genome-wide methylation maps for Proliferating and Senescent cells

(Submitter supplied) Altered DNA methylation and associated destabilization of genome integrity and function is a hallmark of cancer. Replicative senescence imposes a limit on proliferative potential that all cancer cells must bypass. Compared to proliferating cells, senescent cells exhibit marked chromatin re-organization. Here we show by whole-genome single-nucleotide bisulfite sequencing that replicative senescent human cells exhibit widespread alterations in their DNA methylome. more...
Organism:
Homo sapiens
Type:
Methylation profiling by high throughput sequencing
Platform:
GPL11154
9 Samples
Download data: BED, BIGWIG, TXT
Series
Accession:
GSE48580
ID:
200048580
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