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Author(s): Zamble DB; Jacks T; Lippard SJ
Title: p53-dependent and -independent responses to cisplatin in mouse testicular teratocarcinoma cells
Source: PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 95 (11): 6163-6168
Date: 1998 MAY 26
Document Type: Journal : Article
DOI:
Language: English
Comment:
Address: MIT, Dept Chem, Cambridge, MA 02139 USA.
MIT, Ctr Canc Res, Cambridge, MA 02139 USA. MIT, Howard Hughes Med Inst, Dept Biol, Cambridge, MA 02139 USA. Reprint: Lippard, SJ, MIT, Dept Chem, 77 Massachusetts Ave, Cambridge, MA 02139
USA. E-mail:
Author Keywords:
KeyWords Plus: P53-MEDIATED G(1) ARREST; CELLULAR TUMOR-ANTIGEN; HAMSTER OVARY CELLS;
P53 GENE; DNA-DAMAGE; TRANSLATIONAL REGULATION; CYCLE PROGRESSION;
INDUCED APOPTOSIS; HUMAN CANCERS; PROTEIN
Abstract: Testicular cancers respond favorably to chemotherapy with the platinum-containing drug cis-diamminedichloroplatinum(II) (cisplatin). One factor that could explain the efficacy of cisplatin is the low frequency of p53 mutations observed in this tumor type. The present study examines the p53-mediated responses in murine testicular teratocarcinoma cells exposed to the drug. Cisplatin treatment of teratocarcinoma cells with a wild-type p53 gene resulted in accumulation of the p53 protein through posttranscriptional mechanisms; induction of p53 target genes was also observed. Drug treatment resulted in rapid apoptosis in p53-wild-type cells but not in p53(-/-) teratocarcinoma cells. In the latter cells, cisplatin exposure caused prolonged cell cycle arrest accompanied by induction of the p21 gene. Clonogenic assays demonstrated that the p53 mutation did not confer resistance to cisplatin. These experiments suggest that cisplatin inhibits cellular proliferation of testicular teratocarcinoma cells by two possible mechanisms, p53-dependent apoptosis and p53-independent cell cycle arrest.
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