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Identification of microRNAs dysregulated in cellular senescence driven by endogenous genotoxic stress

ABSTRACT: We compared microRNA (miRNA) expression in Ercc1-/- primary mouse embryonic fibroblasts (MEFs) and wild-type (WT) MEFs in 20% O2 and 3% O2 growth conditions to identify miRNAs that drive cellular senescence.

ORGANISM(S): Mus musculus

PROVIDER: GSE48417 | GEO | 2013/06/29

SECONDARY ACCESSION(S): PRJNA209989

REPOSITORIES: GEO

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Identification of microRNAs dysregulated in cellular senescence driven by endogenous genotoxic stress

Project description:We compared microRNA (miRNA) expression in Ercc1-/- primary mouse embryonic fibroblasts (MEFs) and wild-type (WT) MEFs in 20% O2 and 3% O2 growth conditions to identify miRNAs that drive cellular senescence. MicroRNA expression in WT and Erccc1-/- MEFs was measured at passage 3 and passage 7 after growth in 20% and 3% O2. Two independent experiments were performed for each growth condition.

2013-06-29 | E-GEOD-48417 | biostudies-arrayexpress

Identification of microRNAs dysregulated in cellular senescence driven by endogenous genotoxic stress.

Project description: Not available

| S-EPMC3824412 | biostudies-literature

Foxp3 is a key downstream regulator of p53-mediated cellular senescence

Project description:The downstream events and target genes of p53 in senescence responses are not fully understood. Here, we report a novel function of the forkhead transcription factor Foxp3, a key player in mediating T cell inhibitory function, in p53-mediated cellular senescence. Overexpression of Foxp3 in mouse embryonic fibroblasts (MEFs) accelerates senescence, whereas Foxp3 knockdown leads to escape from p53-mediated senescence in p53-expressing MEFs. Consistently, Foxp3 expression resulted in the induction of senescence in epithelial cancer cells, including MCF7 and HCT116. Foxp3 overexpression also increased the intracellular levels of reactive oxygen species (ROS). The ROS inhibitor N-acetyl-L-cysteine rescued Foxp3 expression-induced senescence. Furthermore, the elevated ROS levels that accompanied Foxp3 overexpression were paralleled by an increase in p21 expression. Knockdown of p21 in Foxp3-expressing MEFs abrogated the Foxp3-dependent increase in ROS levels, indicating that Foxp3 acts through p21 induction and subsequent ROS elevation to trigger senescence. Collectively, these results suggest that Foxp3 is a downstream target of p53 that is sufficient to induce p21 expression and ROS production and is necessary for p53-mediated senescence. control and treated samples (human), young passage (p3) or old passage (p7) samples (mouse)

2015-08-13 | E-GEOD-71980 | biostudies-arrayexpress

Proteomics revealed the effects of high O2 stress on nucleic acid metabolism, yellowing and senescence in postharvest broccoli

Project description:Proteomics revealed the effects of high O2 stress on nucleic acid metabolism, yellowing and senescence in postharvest broccoli

2022-08-31 | PXD036422 | iProX

Foxp3 is a key downstream regulator of p53-mediated cellular senescence

Project description:The downstream events and target genes of p53 in the process of senescence are not fully understood. Here, we report a novel function of the forkhead transcription factor Foxp3, which is a key player in mediating T cell inhibitory functions, in p53-mediated cellular senescence. The overexpression of Foxp3 in mouse embryonic fibroblasts (MEFs) accelerates senescence, whereas Foxp3 knockdown leads to escape from p53-mediated senescence in p53-expressing MEFs. Consistent with these results, Foxp3 expression resulted in the induction of senescence in epithelial cancer cells, including MCF7 and HCT116 cells. Foxp3 overexpression also increased the intracellular levels of reactive oxygen species (ROS). The ROS inhibitor N-acetyl-L-cysteine rescued cells from Foxp3-expression-induced senescence. Furthermore, the elevated ROS levels that accompanied Foxp3 overexpression were paralleled by an increase in p21 expression. Knockdown of p21 in Foxp3-expressing MEFs abrogated the Foxp3-dependent increase in ROS levels, indicating that Foxp3 acts through the induction of p21 and the subsequent ROS elevation to trigger senescence. Collectively, these results suggest that Foxp3 is a downstream target of p53 that is sufficient to induce p21 expression and ROS production and is necessary for p53-mediated senescence.

2015-08-13 | GSE71980 | GEO

RNA-seq of H2afj-ko and isogenic WT C57/Bl6-N mouse embryonic fibroblasts in proliferation and after etoposide-induced senescence.

Project description:Determine the effect of knocking out the H2afj gene on the transcriptome of MEFs induced into senescence with etoposide. MEFs were produced from individual H2A.J-ko or isogenic WT C57BL/6-N embryos. 3 different female WT and H2A.J-ko MEFs were used for the transcriptome analyses. MEFs were cultivated in DMEM + Gluta-Max (Gibco 31966) + 10%FBS + pen/strep in a 5% carbon dioxyde and 5% oxygen incubator. MEFs were passed twice before inducing senescence by treatment with 2.5 µM etoposide for 6 days (with media changed after 3 days), followed by 3 days incubation in fresh medium without etoposide.

2020-11-02 | E-MTAB-9704 | biostudies-arrayexpress

Transactivation-deficient p53 Mutants in Ras-induced Cellular Senescence

Project description:As a critical cellular stress sensor, p53 mediates a variety of defensive processes including cell-cycle arrest, apoptosis, and senescence to prevent propagation of hyperproliferative cells or cells with a damaged genome, hence the formation of neoplasia. Transactivation of downstream genes plays an important while sometimes controversial role in regulating these cellular processes. To evaluate the dependence on transcriptional activation in p53’s activities, we generated genetically-modified mouse lines carrying mutations in the transactivation domains (TADs) of p53. These transactivatio-deficient mutants serve as unique reagents to probe the dependence on robust transactivation in p53-mediated cellular functions, as well as the underneath mechanisms. To identify genes differentially regulated by these p53 mutants, we performed gene expression profiling analysis on mouse embryonic fibroblast cells (MEFs) from these mice in the context of oncogenic Ras-induced premature cellular senescence. Mouse embryonic fibroblasts (MEFs) with different p53 genotypes were infected with retroviral H-Ras V12, which induces premature cellular senescence in p53 wild-type MEFs but not in p53 null MEFs. 5 genotypic groups of MEFs were used in the study: (i) p53L25Q/W26S, or "25,26", in which the first TAD (transactivation domain) of p53 is disrupted by the mutation, 5 biological samples; (ii) p53W53Q/F54S, or "53,54", in which the second TAD of p53 is disrupted by the mutation, 3 biological samples; (iii) p53L25Q/W26S/W53Q/F54S, or "QM", in which both TADs or p53 are disrupted, 3 biological samples; (iv) p53 wild-type, or "WT", 6 biological samples; (v) p53 null, or "Null", 6 biological samples.

2011-05-13 | E-GEOD-27901 | biostudies-arrayexpress

Cell Senescence

Project description:Cell Senescence

| PRJNA547762 | ENA

Identification of Dysregulated Competitive Endogenous RNA Networks Driven by Copy Number Variations in Malignant Gliomas.

Project description: Not available

| S-EPMC6827427 | biostudies-literature

Induction of senescence upon loss of the Ash2l subunit of histone H3K4 methyltransferase complexes (RNA-Seq)

Project description:Post-translational modifications of core histones participate in controlling the expression of genes. Methylation of lysine 4 of histone H3 (H3K4) is associated with open chromatin and gene transcription. This histone mark is catalyzed by type 2 lysine methyltransferase (KMT2) complexes. In mammals, these consist of one of 6 different KMT2 enzymes, each associated with 4 core subunits, WDR5, RBBP5, ASH2L and DPY30, which are necessary for catalytic activity. The knockout of Ash2l is embryonically lethal in mice as well as in adult animals when hepatocytes or hematopoietic cells are targeted. To expand on the mechanistic understanding of Ash2l, we have used mouse embryo fibroblasts (MEFs). The knockout of Ash2l resulted in the downregulation of H3K4me3 at a large number of promoters, preferentially those associated with CpG islands, accompanied with broad repression of gene expression. The consequence in MEFs was induction of senescence concomitant with a set of down-regulated signature genes. Thus, although the loss of Ash2l in MEFs has broad and complex consequences on the transcriptional program, the biological consequences were distinct, culminating in senescence.

2022-08-12 | GSE165458 | GEO

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