Transcriptomics

Dataset Information

3

Transcription profiling by array of human p53+ and p53- fibroblasts treated with arsenite


ABSTRACT: 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 µM 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.

INSTRUMENT(S): 418 [Affymetrix]

ORGANISM(S): Homo sapiens  

SUBMITTER: Xiaoqiang Xu  

PROVIDER: E-GEOD-7101 | ArrayExpress | 2007-11-11

SECONDARY ACCESSION(S): GDS2603GSE7101PRJNA98441

REPOSITORIES: GEO, ArrayExpress

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Publications

Exit from arsenite-induced mitotic arrest is p53 dependent.

McNeely Samuel C SC   Xu Xiaogiang X   Taylor B Frazier BF   Zacharias Wolfgang W   McCabe Michael J MJ   States J Christopher JC  

Environmental health perspectives 20060901 9


Arsenic is both a human carcinogen and a chemotherapeutic agent, but the mechanism of neither arsenic-induced carcinogenesis nor tumor selective cytotoxicity is clear. Using a model cell line in which p53 expression is regulated exogenously in a tetracycline-off system (TR9-7 cells) , our laboratory has shown that arsenite disrupts mitosis and that p53-deficient cells [p53(-)], in contrast to p53-expressing cells [p53(+)], display greater sensitivity to arsenite-induced mitotic arrest and apopto  ...[more]

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