Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA359683 | ENA |
REPOSITORIES: ENA
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Project description:p53 is a major tumor suppressor gene that is frequently inactivated in human cancers. One prominent suppressive function of p53 is executing cell cycle arrest, senescence and apoptosis upon stress. Importantly, p53 loss is a prerequisite for cancer development, as is evident in Li-Fraumeni patients and p53 knockout mice. Here we investigated the effect of p53-loss, without induction of additional stress, on DNA replication and genomic instability. We revealed that p53 deficiency leads to enhanced proliferation without upregulating essential pathways requited to support normal DNA replication. This uncoordinated S-phase entry leads to replication-induced genomic instability. Interestingly, DNA replication analyses revealed a novel and non-classical form of replication stress induced by p53-loss, characterized by reduced fork rate progression without the compensation of dormant origin activation. Altogether, the results reveal a non-canonical tumor suppressive role of p53 in regulating DNA replication which safeguards genomic stability, underlying cancer predisposition induced by p53-loss. In order to understand the molecular basis for shp53 non-classical form of replication stress and replication-induced genomic instability, we performed unbiased whole transcriptome analysis of BJ-hTERT control cells in comparison to BJ-hTERT cells expressing shRNA against p53. Our results suggest that shp53 cells fail to upregulate essential pathways required for normal DNA replication.
2025-06-01 | GSE93046 | GEO
Project description:Transcriptional profiling of human BJ fibroblasts comparing control FF shRNA expressing cells vs. BRD7 shRNA expressing cells under two conditions, either untreated or treated with 8uM nutln-3a for 8 hours. This experiment was done using two independent shRNAs targeting BRD7. Nutlin-3a was used to stabilize p53 and induce its transcriptional activity.
2010-07-01 | GSE22607 | GEO
Project description:Oncogene-induced senescence (OIS) is a p53-dependent defence mechanism against uncontrolled proliferation. Consequently, many human tumours harbour p53 mutations while others show a dysfunctional p53 pathway, frequently by unknown mechanisms. We identified BRD7, a bromodomain-containing protein whose inhibition allows full neoplastic transformation in the presence of wild-type p53. Intriguingly, in human breast tumours harbouring wild-type, but not mutant p53, the BRD7 gene locus was frequently deleted and low BRD7 expression was found in a subgroup of tumours. Functionally, BRD7 is required for efficient p53-mediated transcription of a subset of target genes. BRD7 interacts with p53 and p300, and is recruited to target gene promoters, affecting histone acetylation, p53 acetylation, and promoter activity. Thus, BRD7 suppresses tumourigenicity by serving as a p53 cofactor required for efficient induction of p53-dependent OIS. We recorded mRNA expression profiles of BJ primary fibroblasts expressing the oncogene RasV12 and either control vector, one of two BRD7 knockdown vectors, or p53 knockdown vector. In addition, we profiled genome-wide protein DNA interactions for p53 and BRD7 using ChIP-Seq. p53- and BRD7-binding sites were recorded in RasV12-expressing BJ cells; as a control we used knockdown of the gene of interest (BRD7 or p53).
2010-03-14 | E-GEOD-20076 | biostudies-arrayexpress
Project description:Transcriptional profiling of human BJ fibroblasts comparing control FF shRNA expressing cells vs. BRD7 shRNA expressing cells under two conditions, either untreated or treated with 8uM nutln-3a for 8 hours. This experiment was done using two independent shRNAs targeting BRD7. Nutlin-3a was used to stabilize p53 and induce its transcriptional activity. Two-condition experiment, FF shRNA cells vs. BRD7 shRNAs cells in two experimental conditions, either untreated or treated with nutlin-3a.
2010-07-01 | E-GEOD-22607 | biostudies-arrayexpress
Project description:Expression data from BJ-hTERT cells expressing vector, Cyclin E, c-Myc or coexpression of both
| PRJNA139271 | ENA
Project description:We generated H3K9me3 profile of reads and peaks of BJ fibroblasts expressing hTERT and SV40 early region (BJ-HELT cell line).
2018-08-04 | GSE102278 | GEO
Project description:These data support our manuscript "Selective abrogation of S6K2 maps lipid homeostasis as a survival vulnerability in MAPKi-resistant NRAS-mut melanoma". Proteomics was performed for M93-047 melanoma cells expressing vector control, S6K1 shRNA knockdown or S6K2 shRNA knockdown.
2019-02-25 | MSV000083480 | MassIVE
Project description:Aim: identification of differentially expressed genes after LIN-9 depletion.<br> <br> hTERT immortalized human BJ fibroblasts were infected with pMSCV-Blasticidin based retroviruses encoding a shRNA which targets human LIN-9 and the empty vector respectively.<br> After 4 days of selection total RNA was isolated. Cy3 and Cy5 labelled cDNA probes were generated using the CyScribe Post-labelling Kit (Amersham Biosiences).
2006-11-23 | E-MEXP-752 | biostudies-arrayexpress
Project description:exosomes isolated from: HT29+control shRNA; HT29+p53 shRNA; HCT116 WT p53; HCT116 mutant p53; HCT116 null p53; media used as negative control
2018-02-09 | MSV000082047 | MassIVE
Project description:Limited data exists regarding changes of microRNA (miRNA) expression during senescence in human cells and no reports correlate telomerase expression with regulation of senescence-related miRNAs. We used miRNA microarrays to provide a detailed account of miRNA profiles for early passage and senescent human foreskin (BJ) fibroblasts as well as early and late passage immortalized fibroblasts (BJ-hTERT) that stably express the human telomerase reverse transcriptase subunit hTERT. The revelation that miRNA expression changes with extended passaging in BJ-hTERT cells will contribute to a comprehensive understanding of the connections between telomerase expression, senescence and processes of cellular aging.
2010-06-05 | GSE22134 | GEO