Journal
ONCOGENE
Volume 21, Issue 29, Pages 4539-4548Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/sj.onc.1205551
Keywords
Rb; E2F; prohibitin; apoptosis; cell cycle
Funding
- NCI NIH HHS [CA77301] Funding Source: Medline
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Prohibitin, a potential tumor suppressor, is known to induce growth suppression and repress E2F-mediated transcription. These growth regulatory functions of prohibitin require a physical interaction with the Rb protein. We now find that prohibitin protects cells from apoptosis mediated by camptothecin, a topoisomerase I inhibitor. Camptothecin treatment of Ramos B cells leads to the degradation of Rb protein and phosphorylation of its family members, p107 and p130. This correlates with an increase in the levels of cyclin E as well as the kinase activity associated with it. Inactivation of Rb leads to the dissociation and release of free E2F. We find also that E2F activity is induced upon camptothecin treatment, but this increase is absent in prohibitin overexpressing cells. It thus appears that prohibitin may be inhibiting apoptosis by downregulating E2F activity when Rb family members are inactive.
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