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E-GEOD-26262

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

OTHER RELATED OMICS DATASETS IN: PRJNA135101

PROVIDER: E-GEOD-26262 | ExpressionAtlas | 2015-08-12

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-GEOD-26262-analysis-methods.tsv	Tabular
	E-GEOD-26262-atlasExperimentSummary.Rdata	Rdata
	E-GEOD-26262-configuration.xml	Xml
	E-GEOD-26262-percentile-ranks.tsv	Tabular
	E-GEOD-26262.condensed-sdrf.tsv	Tabular

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Pin1/mutant-p53 jointly controlled genes

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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

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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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Project description:MDA-MB-231 are a metastatic triple-negative breast cancer cell line that bears a missense p53 mutation (R280K). We depleted endogenous mutp53 in MDA-MB-231 cells by siRNA transfection, and treated the cells with Tumor Necrosis Factor (TNF)-alpha. Microarray analysis was performed to evaluate the impact of mutant p53 on the transcriptional response triggered by TNFα in these cells. MDA-MB-231 cells transfected with control or p53 siRNA were treated with TNFα for 20 hrs or left untreated. The study comprises four experimental points, each in triplicate.

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Project description:TGFβ 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 TGFβ-dependent cell migration, invasion and metastasis are empowered by mutant-p53. To investigate the specific gene expression program by which mutant-p53 and TGFβ control invasion and metastasis in breast cancer cells, we compared the TGFβ transcriptomic profile of control and mutant-p53 depleted MDA-MB-231 cells. Keywords: expression profiling by array

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

Project description:Mutant p53 can acquires oncogenic properties supporting tumor growth, metastases and chemoresistance, by reprogramming cancer cell transcriptome, proteome and metabolome. To investigate what is the gene expression network regulated by mutant p53, we silenced its expression in MDA-MB-231 Triple Negative Breast Cancer (TNBC) cell line. We then performed gene expression profiling analysis using data obtained from RNA-seq of MDA-MB 231.

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Effect of silencing of p53 on gene expression in MDA-MB 231 TNBC cell line in medium with 100% and medium with 25% of amino acids. [aa]

Project description:Mutant p53 can acquires oncogenic properties supporting tumor growth, metastases and chemoresistance, by reprogramming cancer cell transcriptome, proteome and metabolome. To investigate what is the gene expression network regulated by mutant p53 in condition of limited amino acids availability, we silenced mutant p53 expression in MDA-MB-231 Triple Negative Breast Cancer (TNBC) cell line, grown in medium with 100% and medium with 25% of amino acids. We performed gene expression profiling analysis using data obtained from RNA-seq of MDA-MB 231.

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Project description:In this study, the effect of arginine deprivation on global gene expression in MDA-MB-231 and its ρ0 cells were examined. MDA-MB-231 ρ0 cells lack mitochondrial DNA and therefore have impaired OXPHOS function. Both parental and ρ0 cells were cultured in complete or arginine depleted medium for 48 hours. Comparative transcriptome analysis of both cell lines in complete growth medium versus arginine depleted medium were performed.

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