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Vol. 53, Issue 5, 819-826, May 1998
Cancer Research Campaign Molecular and Cellular Pharmacology
Research Group, We investigated the roles of p53 and Bcl-2 homologues in the induction
of apoptosis by cisplatin and paclitaxel in wild-type p53-expressing
human ovarian carcinoma cells and cisplatin-resistant derivatives that
have lost p53 function. Cisplatin induced apoptosis in parental A2780
but not in cisplatin-resistant A2780/cp70 cells, whereas paclitaxel
induced apoptosis in both cell lines. Immunoprecipitation of p53 using
antibodies specific for p53 conformation (pAb 1620 and pAb 240) showed
that there were no relative changes in p53 conformation before and
after cisplatin treatment in either cell line. A2780/cp70 cells have
lost p53 function, yet they have wild-type p53 gene sequence. However,
A2780/cp70 cells constitutively express more p53 in a form detected by
pAb 240, an antibody that also detects mutant conformations of p53 that
are transcriptionally inactive. There were no changes in levels of
Bcl-2, Bcl-XL, or 24-kDa Bax over 72 hr after exposure to
cisplatin or paclitaxel, but each agent led to up-regulation of Bak and
21-kDa Bax in A2780 cells. Paclitaxel, but not cisplatin, increased Bak
and 21-kDa Bax levels in A2780/cp70 cells. These data suggest that
apoptosis in A2780 and A2780/cp70 is associated with an increased level of Bak and 21 kDa Bax after drug-induced damage and that functional p53
may be required for this effect after cisplatin but not after paclitaxel.
Copyright © 1998 by The American Society for Pharmacology and Experimental Therapeutics
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