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Total RNA-seq from HCT116, MCF7 and SJSA cell lines treated with DMSO and Nutlin

ABSTRACT: To determine effects of p53 activation on steady-state mRNA levels, we performed RNA-seq analysis of colorectal carcinoma cell line HCT116 (p53+/+ and p53 -/-), breast carcinoma line MCF7, and osteosarcoma line SJSA treated with MDM2 inhibitor Nutlin.

ORGANISM(S): Homo sapiens

PROVIDER: GSE86221 | GEO | 2017/08/22

SECONDARY ACCESSION(S): PRJNA340956

REPOSITORIES: GEO

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RNAseq from polysomal RNA harvested from HCT116, MCF7 and SJSA cell lines treated with DMSO and Nutlin

Project description:To determine effects of p53 activation on levels of RNA associated with polysomes, we performed RNA-seq analysis of colorectal carcinoma cell line HCT116, breast carcinoma line MCF7, and osteosarcoma line SJSA treated with MDM2 inhibitor Nutlin.

2017-08-22 | GSE86219 | GEO

p53 ChIP-seq in Nutlin-treated HCT116, MCF7, and SJSA cell lines

Project description:To identify genomic loci occupied by p53, we performed p53 ChIP-seq analysis of colorectal carcinoma cell line HCT116, breast carcinoma line MCF7, and osteosarcoma line SJSA treated with MDM2 inhibitor Nutlin.

2017-08-22 | GSE86164 | GEO

GRO-seq from HCT116, MCF7 and SJSA cell lines treated with DMSO and Nutlin

Project description:To identify loci with transcriptionally engaged RNA polymerase, we performed GRO-seq analysis of colorectal carcinoma cell line HCT116, breast carcinoma line MCF7, and osteosarcoma line SJSA treated with MDM2 inhibitor Nutlin.

2017-08-22 | GSE86165 | GEO

12hr 5-FU treatment vs. DMSO in SJSA cells (from 'A kinase independent role for CDK19 in p53 response')

Project description:The human Mediator complex regulates RNA Polymerase II transcription genomewide. A general factor that regulates Mediator function is the four-subunit Mediator kinase module, which contains either CDK8 or CDK19. Whereas CDK8 has been linked to specific signaling cascades and oncogenesis, the cellular roles of its paralog, CDK19, are poorly studied. To define cellular roles for CDK19, we used osteosarcoma cells (SJSA) that naturally lack endogenous CDK8 protein. Although stable CDK19 knockdown was tolerated in SJSA cells, it caused reduced proliferation vs. control shRNA cells. Global gene expression analyses (RNA-Seq) suggested that defects in cholesterol biosynthesis contributed to reduced proliferation in CDK19 knockdown cells (vs. shCTRL). Notably, proliferation defects were rescued with transient expression of wild-type or kinase-dead CDK19. Using RNA-Seq and other assays, we established a general role for CDK19 in the transcriptional response to 5-fluorouracil (5-FU), an inducer of genotoxic and metabolic stress. These experiments also implicated CDK19 in activation of p53 target genes during 5-FU treatment. To further probe a potential role for CDK19 in the p53 response, SJSA cells (shCDK19 vs. shCTRL) were treated with the p53 activator Nutlin-3. Remarkably, CDK19 was required for SJSA cells to return to a proliferative state following Nutlin-3 treatment, and this effect was kinase-independent. These results implicate CDK19 as a regulator of p53 stress responses and suggest a manifestation of CDK19 knockdown—potentially reduced levels of cholesterol metabolites—blocks cellular resistance to Nutlin-3.

2017-05-09 | GSE89807 | GEO

shRNA screens for mediators of anti-proliferative effects of p53 in SJSA cell line

Project description:To identify genes required for anti-proliferative function of p53 we performed genome-wide and p53TARGET screens in SJSA cells treated with Nutlin.

2017-08-22 | GSE86220 | GEO

Cooperation of Nutlin-3a and a Wip1 inhibitor to induce p53 activity

Project description:Targeting the Mdm2 oncoprotein by drugs has the potential of re-establishing p53 function and tumor suppression. However, Mdm2-antagonizing drug candidates, e. g. Nutlin-3a, often fail to abolish cancer cell growth sustainably. To overcome these limitations, we inhibited Mdm2 and simultaneously a second negative regulator of p53, the phosphatase Wip1/PPM1D. When combining Nutlin-3a with the Wip1 inhibitor GSK2830371 in the treatment of p53-proficient but not p53-deficient cells, we observed enhanced phosphorylation (Ser 15) and acetylation (Lys 382) of p53, increased expression of p53 target gene products, and synergistic inhibition of cell proliferation. Surprisingly, when testing the two compounds individually, largely distinct sets of genes were induced, as revealed by deep sequencing analysis of RNA. In contrast, the combination of both drugs led to an expression signature that largely comprised that of Nutlin-3a alone. Moreover, the combination of drugs, or the combination of Nutlin-3a with Wip1-depletion by siRNA, activated p53-responsive genes to a greater extent than either of the compounds alone. Simultaneous inhibition of Mdm2 and Wip1 enhanced cell senescence and G2/M accumulation. Taken together, the inhibition of Wip1 might fortify p53-mediated tumor suppression by Mdm2 antagonists.

2016-05-02 | GSE80716 | GEO

Genome-wide map of p53 binding sites by ChIP-seq in human lymphoblastoid cell lines treated with nutlin-3

Project description:We have used chromatin immune-precipitation with parallel sequencing (ChIP-Seq) technology to identify genome-wide p53 binding in human lymphoblastoid cell lines treated with a MDM2 inhibitor nutlin-3 ChIP-Seq analysis of p53 binding sites in human lymphoblastoid cells treated with nutlin-3 or vehicle

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Nutlin-3 treatment of B-CLL

Project description:Background: p53 plays a key role in determining the clinical features of B cell chronic lymphocytic leukemia (CLL). Disruption of p53 by point mutations, deletion at 17p13, or both, occurs in a fraction of cases at diagnosis and predicts poor survival and chemorefractoriness. In cells with functional p53, p53 activity is inhibited through interaction with MDM2. In fact, p53 can be activated upon exposure of cells to inhibitors of p53/MDM2 interaction, like Nutlins. Exposure of CLL cells to Nutlin-3 is effective in raising the levels of p53 protein with subsequent induction of cell cycle arrest and/or apoptosis, independently of the most relevant prognostic markers. Specific gene-sets and GEP were documented to be associated with response or resistance to Nutlin-3 exposure in p53(wt) or p53(del/mut) CLL. These findings may help to identify novel molecular targets for CLL therapy. Aim: to analyze the gene expression profile (GEP) induced by Nutlin-3 exposure in primary CLL cells from p53(wt) and p53(del/mut) cases. Methods: purified cells from 24 PB CLL samples, all characterized for IGHV mutational status, CD38 and ZAP-70 and p53 mutations (16 p53(wt) CLL, 8 p53(del/mut) CLL of which 6 with del17p13 and p53 mutations, 1 with del17p13 alone, and 1 with p53 mutations alone), were exposed to 10 uM Nutlin-3 for 24 hours. GEP was performed using a dual labelling strategy; the differential expression of the below reported genes were validated by quantitative real-time PCR. specific gene-sets and GEP were documented to be associated with response or resistance to Nutlin-3 exposure in p53(wt) or p53(del/mut) CLL. These findings may help to identify novel molecular targets for CLL therapy.

2009-11-11 | GSE18971 | GEO

RNAseq analysis for transcriptomes of colon cancer cell line HCT116 upon p53 and/or iASPP knockdown with or without nutlin treatment

Project description:The tumor suppressor p53 plays a critical role in the cellular response to various stresses, including DNA damage, hypoxia, nutrition starvation, and oncogene activation. However, wild-type p53 function was largely impaired in cancer cells, one of the reasons is the inhibition by p53 negative regulating proteins (iASPP, MDM2 etc.). To globally evaluate the transcriptome inhibited by iASPP and the potent synergy of co-inhibiting MDM2, we performed RNAseq analysis in colon cancer cell line HCT116 upon p53 or iASPP knockdown with or without Nutlin-3 treatment.

2022-10-29 | GSE139546 | GEO

RNA-seq timecourse of p53 activation with Nutlin-3a in IMR90 cells

Project description:To investigate the dynamics of the p53 response, we treated IMR90 cells with Nutlin-3a, a small molecule that inhibits the interaction between p53 and its inhibitor Mdm2, for 6, 9, or 12 hours.

2020-10-31 | GSE139003 | GEO

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