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Clinical Cancer Research, Vol 4, Issue 1 251-259, Copyright © 1998 by American Association for Cancer Research
ARTICLES |
RD Meng, H Shih, NS Prabhu, DL George and WS el-Deiry
Laboratory of Molecular Oncology and Cell Cycle Regulation, University of Pennsylvania School of Medicine, Philadelphia 19104, USA.
Oncoprotein MDM2 inhibits p53-dependent cell cycle arrest and apoptosis. MDM2-overexpressing human cancer cell lines (n = 3) were found to be resistant to growth inhibition after infection by p53-expressing adenovirus (Ad-p53), as compared to low MDM2-expressing tumors (n = 3), in vitro. The growth of MDM2-overexpressing tumors, however, was inhibited by p21-expressing adenovirus (Ad-p21) infection, and the cyclin-dependent kinase-inhibitory region of p21 was sufficient to bypass the MDM2-p53 feedback loop. The phosphorylation state of Rb correlated with the response to either p53 or p21 gene therapy. MDM2-overexpressing cancer cells infected by Ad-p21 also developed a quiescent large-cell morphology. The results suggest that MDM2-mediated resistance to p53 may be bypassed by p21 and that the Rb phosphorylation state may predict the effects on growth after Ad-p53 or Ad-p21 infection.
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