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

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 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.

ORGANISM(S): Homo sapiens

SUBMITTER: Xiaoqiang Xu

PROVIDER: E-GEOD-7101 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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

<h4>Background</h4>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 mitoti ...[more]

PMID: 16966095

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