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Profiling of p53-responsive genes in human breast cancer cells harboring endogenous ts-p53 E285K

ABSTRACT: The ts-p53 E285K protein is a rare p53 mutant with temperature-sensitive (ts) loss of function characteristics. In cancer cells, which express ts-p53 E285K intriniscally, endogenous wild type p53 activity is reconstituted by appropriate cultivation temperature (permissive condition). At non-appropriate cultivation temperature (restrictive condition) this p53 mutant is inactive. The present study took advantage of this mechanism and employed IPH-926 lobular breast cancer cells and BT-474 ductal breast cancer cells, which both harbor endogenous ts-p53 E285K, for the transcriptional profiling of p53-responsive genes. This new approach eliminated the need for genetic modification or cytotoxic stimulation to achive a p53 response in the cells being investigated .

ORGANISM(S): Homo sapiens

PROVIDER: GSE35006 | GEO | 2012/12/31

SECONDARY ACCESSION(S): PRJNA151175

REPOSITORIES: GEO

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Profiling of p53-responsive genes in human breast cancer cells harboring endogenous ts-p53 E285K

Project description:The ts-p53 E285K protein is a rare p53 mutant with temperature-sensitive (ts) loss of function characteristics. In cancer cells, which express ts-p53 E285K intrinsically, endogenous wild type p53 activity is reconstituted by appropriate cultivation temperature (permissive condition). At non-appropriate cultivation temperature (restrictive condition) this p53 mutant is inactive. The present study took advantage of this mechanism and employed IPH-926 lobular breast cancer cells and BT-474 ductal breast cancer cells, which both harbor endogenous ts-p53 E285K, for the transcriptional profiling of p53-responsive genes. This new approach eliminated the need for genetic modification or cytotoxic stimulation to achive a p53 response in the cells being investigated . Three subseqent passages of IPH-926 lobular breast cancer cells (harboring ts-p53 E285K) were seeded into two parallel culture dishes each and were allowed to adopt to restrictive and permissive condition for 24 h before analysis on Affymetrix U133 Plus 2.0 microarrays. Subsequently, this experiment was repeated with BT-474 ductal breast cancer cells (also harboring ts-p53 E285K). To gate out non-specific temperature effects, the same experiment was also performed with MCF-7 breast cancer cells (harboring wt p53). Probe sets differentially expressed at restrictive versus permissive condition in MCF-7 were considered as non-specifically regulated. These probe sets were excluded from the final statistical analysis of IPH-926 and BT-474 expression data. response to restored p53 activity

2012-12-31 | E-GEOD-35006 | biostudies-arrayexpress

Identification of temperature-sensitive (TS) p53 mutations and potassium antimony tartrate (PAT)-treatable p53 mutations in mammalian U937 (free of endogenous p53) cells using a systematic p53 mutation library

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Project description:To identified TS p53 mutations and PAT-treatable p53 mutations in mammalian U937 cells.

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E-GEOD-35006

Project description:Profiling of p53-responsive genes in human breast cancer cells harboring endogenous ts-p53 E285K

2015-08-18 | E-GEOD-35006 | ExpressionAtlas

McKay reversible p53 response

Project description:Reversible p53 activation using a temperature variant of p53

2012-04-30 | E-MEXP-3224 | biostudies-arrayexpress

p53 independent TAF6delta target genes.

Project description:To elucidate the impact of TAF6d on cell death and gene expression, here we have employed modified antisense oligonucleotides to enforce expression of endogenous TAF6d. The induction of endogenous TAF6d triggered apoptosis in tumor cell lines, including cells devoid of p53. Microarray experiments revealed that TAF6d activates gene expression independently of cellular p53 status. Our data define TAF6d as a pivotal node in a signaling pathway that acts immediately downstream of p53 to control gene expression programmes and apoptosis. Keywords: Treatment with splice site switching antisense oligonucleotides, induction of apoptosis Biological triplicates, 4 conditions: isogenic p53+/+ and -/- cells; control oligonucleotide, TAF6 AS2 oligonucleotide

2008-06-26 | E-GEOD-10795 | biostudies-arrayexpress

Transcription profiling of human p53+ and p53- fibroblasts treated with arsenite reveals exit from arsenite-induced mitotic arrest is p53 dependent

Project description:Microarray data from G2-synchronized p53(+) and p53(-) fibroblasts before and after 3 h release from cell cycle blockade in the presence of 5 uM sodium arsenite. Experiment Overall Design: Cells expressing p53 from a tet-off regulated construct were synchronized in G2 with a two-step procedure using 24 h aphidicolin treatment for initial G1 synchronization and 12 h of Hoechst 33342 to effect a G2 blockade. During Hoechst treatment, tetracycline was added to suppress p53 in half the cultures. Cells were then released into media containing 5 ÂµM sodium arsenite and the appropriate concentration of tetracycline to maintaining p53 expression. mRNAs were collected at 0 h and 3 h after release from G2 synchrony.

2007-11-11 | E-GEOD-7101 | biostudies-arrayexpress

Homo sapiens

Project description:Profiling of p53-responsive genes in human breast cancer cells harboring endogenous ts-p53 E285K

| PRJNA151175 | ENA

p53 independent TAF6delta target genes.

2008-06-26 | GSE10795 | GEO

Expression data from mutant p53 breast cancer cell line SK-BR-3

Project description:Tumor associated mutant p53 proteins often gain new functions for tumorigenesis and tumor progression. It has been shown that mutant p53 can transcriptionally regulate a group of genes, which in turn contributes to mutant p53 gain of function. A mutant p53 interacting protein Pontin binds to mutant p53 and promotes its gain of function. This experiment tests whether the interaction of Pontin with mutant p53 regulates the transcriptional activity of mutant p53. We used a breast cancer cell line containing endogenous mutant p53 (SK-BR-3) with or without knockdown of mutant p53 by shRNA to identify genes regulated by mutant p53. We then knocked down endogenous Pontin in SK-BR-3 cells, and compared the transcriptional levels of these genes in cells with and without mutant p53 knockdown to investigate the effect of Pontin on mutant p53-dependent transcriptional regulation.

2015-06-01 | GSE58140 | GEO

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