Expression of wild-type p53 stimulates an increase in both Bax and Bcl-xL protein content in HT29 cells
Merchant, A.K.; Loney, T.L.; Maybaum, J.
Oncogene 13(12): 2631-2637
1996
ISSN/ISBN: 0950-9232 PMID: 9000137 Document Number: 468399
It has been shown previously that wild-type p53 activity can simultaneously up-regulate Bax, a protein which predisposes cells to programmed cell death (PCD), and down-regulate Bcl-2, a protein which antagonizes PCD. These findings have been interpreted to suggest that correction of the mutant p53 status of some tumor cells may be a means of increasing their sensitivity to chemotherapeutic agents, by increasing their likelihood of undergoing PCD. We show here that when wild-type p53 activity is expressed in HT29 human colon cancer cells by use of a temperature sensitive p53 mutant, Bax levels rise, but so do levels of Bcl-X-L, protein. These observations indicate that Bcl-2 and Bcl-X-L, are regulated differently in response to wild-type p53 activity and that, while correction of mutant p53 phenotype may effectively kill cells having Bcl-2 as their major defense against PCD, this is not necessarily the case in cells using Bcl-X-L as their primary defense.