Senescence associated gene signatures
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ABSTRACT:
PROVIDER: PRJNA811141 | ENA |
REPOSITORIES: ENA
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Project description:Gene expression signatures associated with PI3Kα-induced senescence
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Project description:We set out to characterize the transcriptional heterogeneity of the senescence program using a large number of whole-transcriptome sequencing datasets generated by us or publicly available. We identify a number of senescence transcriptional signatures associated to specific stresses or cell types. We also merge all the studies to identify and validate the genes that are universally differentially regulated during senescence.
2017-11-22 | E-MTAB-5403 | biostudies-arrayexpress
Project description:To investigate the mechanisms of PI3Kα-induced senescence, we performed a gene expression microarray analysis with MCF-10A/H and parental MCF-10A cells.
2018-11-28 | GSE123014 | GEO
Project description:Cellular senescence is a stable cell growth arrest that is characterized by silencing of proliferation-promoting genes through compaction of individual chromosomes into senescence-associated heterochromatin foci (SAHF). Paradoxically, senescence is also accompanied by increased expression of certain secreted factors such as cytokines and chemokines, known as senescence-associated secretory phenotype (SASP). How SASP genes are excluded from SAHF-mediated global gene silencing remains unclear. Here we report that HMGB2 orchestrates the chromatin landscape of SASP gene loci. HMGB2 preferentially localizes to SASP gene loci during senescence. Loss of HMGB2 during senescence blunts SASP gene expression by allowing for spreading of repressive heterochromatin into SASP gene loci. This correlated with incorporation of SASP gene loci into SAHF. Our results establish HMGB2 as a novel master regulator that orchestrates SASP through preventing heterochromatin spreading to allow for exclusion of SASP gene loci from a global heterochromatin environment during senescence.
2016-10-11 | GSE85057 | GEO
Project description:Noncoding RNAs include small transcripts, such as microRNAs and piwi-interacting RNAs, and a wide range of long noncoding RNAs (lncRNAs). Although many lncRNAs have been identified, only a small number of lncRNAs have been characterized functionally. Here, we sought to identify lncRNAs differentially expressed during replicative senescence. We compared lncRNAs expressed in proliferating, early-passage, 'young' human diploid WI-38 fibroblasts [population doubling (PDL) 20] with those expressed in senescent, late-passage, 'old' fibroblasts (PDL 52) by RNA sequencing (RNA-Seq). Numerous transcripts in all lncRNA groups (antisense lncRNAs, pseudogene-encoded lncRNAs, previously described lncRNAs and novel lncRNAs) were validated using reverse transcription (RT) and real-time, quantitative (q)PCR. Among the novel senescence-associated lncRNAs (SAL-RNAs) showing lower abundance in senescent cells, SAL-RNA1 (XLOC_023166) was found to delay senescence, because reducing SAL-RNA1 levels enhanced the appearance of phenotypic traits of senescence, including an enlarged morphology, positive β-galactosidase activity, and heightened p53 levels. Our results reveal that the expression of known and novel lncRNAs changes with senescence and suggests that SAL-RNAs play direct regulatory roles in this important cellular process. RNA was extracted from both young and senescent WI-38 cells and used for total RNA-Seq.
2016-02-08 | E-GEOD-77675 | biostudies-arrayexpress
Project description:We used parkin âoverexpressing MRC5 fibroblasts to investigate the role of mitochondria deficiency on senescence-associated gene expression. RNA-seq analysis on proliferating and senescent Parkin-expressing MRC5 fibroblasts treated with CCCP (treated) or DMSO (Untreated).
2016-01-12 | E-GEOD-76125 | biostudies-arrayexpress
Project description:Cellular senescence is a tumor-suppressive program that involves chromatin reorganization and specific changes in gene expression that trigger an irreversible cell-cycle arrest. We have examined the effect of suppressing the histone demethylases Jarid1a and Jarid1b on the senescence-associated gene expression signatures. Human fibroblast (IMR90) cells were infected with retroviral vectors expresssing shRNA targeting Jarid1a, Jarid1b or both, and triggered to undergo quiescence by removal of serum or senescence by over-expression of activated ras (Hrasv12).
2013-01-31 | E-GEOD-43920 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the SubSeries listed below. Oncogene-induced senescence (OIS) and therapy-induced senescence (TIS), while tumor-suppressive, also promote procarcinogenic effects by activating the DNA damage response (DDR), which in turn induces inflammation. This inflammatory response prominently includes an array of cytokines known as the senescence-associated secretory phenotype (SASP). Previous observations link the transcription-associated methyltransferase and oncoprotein MLL1 to the DDR, leading us to investigate the role of MLL1 in SASP expression. Our findings reveal direct MLL1 epigenetic control over proproliferative cell cycle genes: MLL1 inhibition represses expression of proproliferative cell cycle regulators required for DNA replication and DDR activation, thus disabling SASP expression. Strikingly, however, these effects of MLL1 inhibition on SASP gene expression do not impair OIS and, furthermore, abolish the ability of the SASP to enhance cancer cell proliferation. More broadly, MLL1 inhibition also reduces âSASP-likeâ inflammatory gene expression from cancer cells in vitro and in vivo independently of senescence. Taken together, these data demonstrate that MLL1 inhibition may be a powerful and effective strategy for inducing cancerous growth arrest through the direct epigenetic regulation of proliferation-promoting genes and the avoidance of deleterious OIS- or TIS-related tumor secretomes, which can promote both drug resistance and tumor progression. Previously published samples GSM1135046, GSM1135044, GSM1135047, and GSM1135045 were also studied in this investigation and appear in GSE36641. This did not involve re-sequencing or re-alignment, nor any other deviation from the data protocols in that series. Refer to individual Series
2016-02-22 | E-GEOD-78142 | biostudies-arrayexpress
Project description:We used parkin –overexpressing MRC5 fibroblasts to investigate the role of mitochondria deficiency on senescence-associated gene expression.
2016-01-12 | GSE76125 | GEO
Project description:ADAM19 Mediates Cellular Senescence and the Senescence-Associated Secretory Phenotype
2020-04-03 | MSV000085224 | MassIVE