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Pin1/mutant-p53 jointly controlled genes

ABSTRACT: To investigate the specific gene expression program by which mutant-p53 and Pin1 control invasion and metastasis in breast cancer cells, we compared the transcriptomic profile of control, mutant-p53 depleted or Pin1 depleted MDA-MB-231 cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE26262 | GEO | 2011/05/30

SECONDARY ACCESSION(S): PRJNA135101

REPOSITORIES: GEO

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Pin1/mutant-p53 jointly controlled genes

Project description:To investigate the specific gene expression program by which mutant-p53 and Pin1 control invasion and metastasis in breast cancer cells, we compared the transcriptomic profile of control, mutant-p53 depleted or Pin1 depleted MDA-MB-231 cells. MDA-MB-231 cells were transfected twice with siRNA against Pin1, p53 or LacZ as a control. Transfections were performed by using Lifofectamine 2000 (Invitrogen) according to manufacture's procedure. Forty-eight hours after second transfection, samples were then processed for total RNA extraction and hybridization on Affymetrix microarrays. Three biological replicas (A, B, C) were used for each of the three conditions, for a total of 9 samples

2011-05-30 | E-GEOD-26262 | biostudies-arrayexpress

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Selective inhibition of Pin1 with a covalent small molecule targeting its catalytic domain

Project description:From a mechanism-based screening we have identified a novel Pin1 suicide inhibitor, KPT-6566, able to selectively inhibit Pin1 and target it for degradation. We have performed a transcriptiomic analysis comparing Pin1 specific RNA interference in MDA-MB 231 cells with KPT-6566 treatment to assess specificity of the KPT-6566 towards Pin1.

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shRNAi profiling of human MDA-MB-231 cells expressing anti-p53 (shp53) short-hairpin RNAs treated with TFGbeta or control

Project description:TGFÎ² ligands act as tumor suppressors in early stage tumors but are paradoxically diverted into potent prometastatic factors in advanced cancers. The molecular nature of this switch remains enigmatic. We now show that TGFÎ²-dependent cell migration, invasion and metastasis are empowered by mutant-p53. To investigate the specific gene expression program by which mutant-p53 and TGFÎ² control invasion and metastasis in breast cancer cells, we compared the TGFÎ² transcriptomic profile of control and mutant-p53 depleted MDA-MB-231 cells. Experiment Overall Design: MDA-MB-231 cells, stably expressing either control (shGFP) or anti-p53 (shp53) short-hairpin RNAs, were left untreated or treated with TGFbeta. Samples were then processed for total RNA extraction and hybridization on Affymetrix microarrays. Four biological replicas (A, B, C, D) were used for each of the 4 conditions (1: untreated control; 2: TGFbeta treated control; 3: untreated p53-depleted cells; 4: TGFbeta treated mutant-p53-depleted cells), for a total of 16 samples.

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E-GEOD-26262

Project description:Gene expression profile of mutant-p53 depleted or Pin1 depleted MDA-MB-231 cells

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Effect of silencing of p53 on gene expression in MDA-MB 231 TNBC cell line. [sip53]

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