MRNA expression profiling of DNA damage-induced senescent cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE168994 | GEO | 2021/03/17
REPOSITORIES: GEO
Similar Datasets
Project description:We have generated ABCA1 knockout cells using CRISPR/Cas9 system and expanded single cell clones for gene expression profiling. To identify differentially expressed genes during cellular senescence in wild-type and ABCA1 knockout cells, we performed transcriptional profiling with RNA sequencing (RNA-seq) before and after senescence induction using a stress-induced senescence model (bleomycin-induced senescence).
2023-01-15 | GSE222676 | GEO
Project description:Activation of oncogene signaling in primary cells generally results in cellular senescence. This process is not only considered to be tumor-protective, but also irreversible. However, if senescence induction can be circumvented, e.g. by additional genetic or epigenetic changes, tumor progression occurs. An in-vivo example for oncogene-induced senescence are human nevus cells, most of which bear oncogenic mutations in RAS/RAF/MAPK pathway genes. Here, we show that expression of the human melanoma oncogene N-RAS61K in cultured pigment cells initially induces OIS characterized by a highly multinucleated phenotype. Surprisingly, after prolonged periods of oncogene expression, mononucleated cells emerge from the multinucleated cells. They are highly proliferative, anoikis-resistent and induce fast growing and metastatic melanoma upon transplantation into nude mice. During long-term oncogene expression and the corresponding development of anoikis iresistance, expression of melanocyte-specific genes is lost. Our data demonstrate that the induction of oncogene-induced senescence is not just a failsafe escape mechanism, but also provides a source for highly aggressive tumor cells. total samples analysed are 4
2014-01-20 | E-GEOD-27010 | biostudies-arrayexpress
Project description:For studing dynamic transcriptome profiling in DNA damage-induced cellular senescence and transient cell-cycle arrest, samples were treated with the DNA-damaging agent bleomycin at 0 ug/ml, 2 ug/ml and 40 ug/ml for 2 h. High-resolution time course analysis of gene expression in DNA damage-induced cellular senescence and transient cell-cycle arrest was used to explore the transcriptomic differences between different cell fates after DNA damage response.
2018-03-27 | GSE112068 | GEO
Project description:Mouse skin fibroblasts (MSFs) were obtained from a FASST (Fibroblasts Accelerate Stromal-Supported Tumorigenesis) mouse. This mouse model allows for spatial and temporal control for senescence induction by using a stromal specific Cre-recombinase driven by the pro-collagen-alpha II promoter. The stromal specific Cre activates expression of the p27IRESGFP transgene that is expressed from the ROSA locus. We cultured the MSFs in vitro, induced senescence using 10uM tamoxifen added to the media. Non-senescent cells were treated with equal volume of vehicle alone (ethanol). Upon tamoxifen treatment, cells were moved to a modular incubation chamber and maintained at 3% oxygen at 37 degrees celcius for 12 days total before collection. At the time of collection, cells were trypsynized and pelleted by centrifugation. The cells were lysed using Trysol reagent and RNA was isolated using a RiboPure RNA isolation kit (Ambion).
2017-02-10 | GSE78128 | GEO
Project description:Cellular senescence is defined as permanent growth arrest induced by various stresses. Although the transcriptional activity of p53 is essential for senescence induction, the downstream genes that are crucial for senescence remain unsolved. We developed an experimental system in which either senescence or apoptosis is specifically induced in the same cell line (hepatocarcinoma HepG2 cells having the intact p53 gene) by altering concentrations of a DNA-damaging drug and compared gene expression profiles by using microarray analysis to distinguish genes specific for senescence from those universally respond to DNA damage. When we compared the expression profiles at low versus high doses of etoposide, 20 genes were found to be differentially upregulated by more than 2-fold at a low dose of etoposide, which are expected to function in senescence induction. Microarray results were further confirmed by qPCR.
2017-02-09 | GSE61110 | GEO
Project description:Senescent cells are a major cause of organismal aging and a key target for anti-aging therapies. Persistent DNA damage signaling is a primary driver of the induction and maintenance of cellular senescence. However, many DNA damaging stimuli that induce senescence, such as irradiation or transient exposure to genotoxic drugs, are transient. The mechanisms underlying persistent damage signaling in senescent cells, and why senescent cells fail to repair damaged DNA, remain unknown. Here, we were able to assess the mechanisms underlying persistence of DNA damage and senescence maintenance by designing a precisely controllable senescence system that does not require potent stressors to induce senescence. We demonstrate that sustained mTORC1 signaling in senescent cells causes gradually accumulating DNA damage and an inflammatory response that maintains cell-cycle arrest. Markedly, activation of E2F transcription, which promotes expression of DNA repair proteins, can reverse accumulated DNA damage. Thus, persistent DNA damage signaling arises in senescent cells by uncoupling of mTORC1 and E2F signaling, whereby prolonged mTORC1 activity causes gradually increasing DNA damage that cannot be sufficiently repaired without induction of protective E2F target genes.
2023-06-01 | GSE153683 | GEO
Project description:mRNA expression profiling of DNA damage-induced senescent cells
| PRJNA714876 | ENA
Project description:Activation of oncogene signaling in primary cells generally results in cellular senescence. This process is not only considered to be tumor-protective, but also irreversible. However, if senescence induction can be circumvented, e.g. by additional genetic or epigenetic changes, tumor progression occurs. An in-vivo example for oncogene-induced senescence are human nevus cells, most of which bear oncogenic mutations in RAS/RAF/MAPK pathway genes. Here, we show that expression of the human melanoma oncogene N-RAS61K in cultured pigment cells initially induces OIS characterized by a highly multinucleated phenotype. Surprisingly, after prolonged periods of oncogene expression, mononucleated cells emerge from the multinucleated cells. They are highly proliferative, anoikis-resistent and induce fast growing and metastatic melanoma upon transplantation into nude mice. During long-term oncogene expression and the corresponding development of anoikis iresistance, expression of melanocyte-specific genes is lost. Our data demonstrate that the induction of oncogene-induced senescence is not just a failsafe escape mechanism, but also provides a source for highly aggressive tumor cells.
2014-01-20 | GSE27010 | GEO
Project description:To examine effects of COPI depletion on senescence transcriptional signatures we generated cell lines (IMR90 or IMR90 ER:RAS cells) with inducible 2 COPI shRNAs or control shRNAs and induced to senesce with either treatment with Bleomycin or 4OHT treatment. Transcriptional analysis was performed 3 days after induction of doxycycline inducible harpins and 10 days after senescence induction.
2023-09-28 | GSE224070 | GEO
Project description:Time-course transcriptional profiling of senescing barley leaves. In this model, the senescence process was induced by continued incubation of the seedlings in darkness. Plant samples for the expression analysis were collected before senescence induction (Day 0) and after 3,7 and 10 days of incubation in the dark. The goal was to find the genes differentially expressed during the senescence process . Additionally, a list of the genes with the invariant expression was generated as a resource for selecting references suitable for qPCR or ddPCR experiments. Time-course experiment, two-color, common reference design. All of the data were obtained from material collected in three independent, time-separated leaf senescing experiments (biological replicates). In each replicate, samples from senescing leaves (3 Days, 7 Days, 10 Days) were compared to samples collected before the senescence induction (Day 0). 3 biological replicates.Cy5-labeled samples of interest (Day 0, Day 3, Day 7 and Day 10 from each biological replicate) were each hybridized against a Cy3-labeled common reference (RNA pool of all samples) on a total of 12 microarrays.
2014-10-22 | E-GEOD-62539 | biostudies-arrayexpress