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Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of human colorectal carcinoma-derived cell lines, p53 -/-, +/-, +/+ at 0 and 12 hrs after growth arrest

ABSTRACT: Human colorectal carcinoma-derived cell lines, p53 -/-, +/-, +/+ at 0 and 12 hrs after growth arrest.

ORGANISM(S): Homo sapiens

SUBMITTER: Fred Wright

PROVIDER: E-GEOD-90 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Gene expression profiling of isogenic cells with different TP53 gene dosage reveals numerous genes that are affected by TP53 dosage and identifies CSPG2 as a direct target of p53.

Yoon Heejei H Liyanarachchi Sandya S Wright Fred A FA Davuluri Ramana R Lockman Janet C JC de la Chapelle Albert A Pellegata Natalia S NS

Proceedings of the National Academy of Sciences of the United States of America 20021115 24

TP53 does not fully comply with the Knudson model [Knudson, A. G., Jr. (1971) Proc. Natl. Acad. Sci. USA 68, 820-823] in that a reduction of constitutional expression of p53 may be sufficient for tumor predisposition. This finding suggests a gene-dosage effect for p53 function. To determine whether TP53 gene dosage affects the transcriptional regulation of target genes, we performed oligonucleotide-array gene expression analysis by using human cells with wild-type p53 (p53 +/+), or with one (p53 ...[more]

PMID: 12438652

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The effect of Δ122p53, a Δ133p53α-like isoform, on global gene expression in response to DNA damage in mouse splenocytes

Project description:The p53 protein is a pivotal tumor suppressor that is frequently mutated in many human cancers, although precisely how p53 prevents tumors is still unclear. To add to its complexity several isoforms of human p53 have now been reported. The Δ133p53α isoform is generated from an alternative transcription initiation site in intron 4 of the p53 gene (TP53) and lacks the N-terminus. Elevated expression of Δ133p53α has been observed in a variety of tumors. To explore the functions of Δ133p53α, we created a mouse expressing an N-terminal deletion mutant of p53 (Δ122p53) that corresponds to Δ133p53α. Δ122p53 mice show decreased survival and a different and more aggressive tumor spectrum compared to p53 null mice, implying that Δ122p53 is a dominant oncogene. Consistent with this, Δ122p53 also confers a marked proliferative advantage on cells and reduced apoptosis. In addition to tumor development Δ122p53 mice show a profound pro-inflammatory phenotype having increased serum concentrations of interleukin (IL)-6 and other pro-inflammatory cytokines and lymphocyte aggregates in the lung and liver as well as other pathologies. Based on these observations, we propose that human Δ133p53α also functions to promote cell proliferation and inflammation, one or both of which contribute to tumor development. Total RNA was isolated from pooled splenocytes from four 5-6 week old mice with different p53 status (wild type, p53-/-, or Δ122p53) subjected to DNA damaging or control treatments.

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