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PMID: 14508115 Published · ppublish English Journal Article

Global genechip profiling to identify genes responsive to p53-induced growth arrest and apoptosis in human lung carcinoma cells.

Cancer biology & therapy ·Vol. 2 ·No. 4 ·2003-00-00 ·Pages 406-15

Robinson M, Jiang P, Cui J, Li J, Wang Y, Swaroop M, Madore S, Lawrence TS, Sun Y

Abstract

To identify critical genes that mediate p53-induced growth arrest and apoptosis at a global level, we profiled a human lung carcinoma cell model in which cells undergo growth arrest and apoptosis in a p53 and DNA damage-dependent manner. Profiling of the Affymetrix human HG-U1333 GeneChip, covering the entire human transcriptome, revealed about 3, 000 unique genes either induced or repressed during p53-induced growth arrest or apoptosis, respectively. A total of 1, 057 genes, including many well-known p53 targets, responded to both conditions. A mini apoptotic protein database was generated from 3, 033 unique apoptosis responsive genes. Analysis of this database yielded 23 proteins with a pro-apoptotic BH3 domain and three with anti-apoptotic BIR2/BIR3 domains, including well-known p53 targets: Bax, Puma, Noxa and survivin. In addition, 14 mitochondrial proteins were identified that contain a pro-apoptotic AVPI-like motif, and 15 proteins were identified that contain a DAVPI-like domain with the potential of being cleaved by caspases during apoptosis to release the AVPI motif. Many of the genes we identified with these domains do contain p53-binding sites either in the promoter or in the first three introns, suggesting a high probability of being direct p53 targets. Pathway analysis revealed that p53 might control the Wnt pathway through transcriptional regulation of some of its components. Thus, global chip profiling coupled with bioinformatics analysis is a powerful tool in identification of genes critical for p53-induced apoptosis. Further characterization of these genes will lead to a better understanding of the mechanism of p53 action and p53 regulation of other signaling pathways. It will also provide novel cancer drug targets for further validation.

MeSH Terms
Apoptosis/genetics Binding Sites Cell Cycle/genetics Cell Division Computational Biology Gene Expression Profiling Gene Expression Regulation, Neoplastic Humans Lung Neoplasms/genetics,metabolism,pathology Neoplasm Proteins/genetics Oligonucleotide Array Sequence Analysis Promoter Regions, Genetic/genetics Tumor Cells, Cultured Tumor Suppressor Protein p53/genetics,physiology
Chemicals
Neoplasm Proteins Tumor Suppressor Protein p53
Authors & Affiliations
9 authors, click to expand affiliations / ORCID
Robinson Megan
Departments of Molecular Sciences and Technologies; Pfizer Global Research and Development; Ann Arbor Laboratories; Ann Arbor, Michigan USA. agudkov56@yahoo.com
Jiang Ping
Cui Jenny
Li Jun
Wang Yuli
Swaroop Manju
Madore Steve
Lawrence Theodore S
Sun Yi
Article Info
Journal
Cancer biology & therapy
Abbr.
Cancer Biol Ther
ISSN
1538-4047
Published
2003-00-00
Pages
406-15
Language
English
Region
United States
NLM ID
101137842
Subset
IM
Corrections
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