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Jefferson Cancer Instiute and Jefferson Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania 19107
bcl-2 and p53 gene products have been both linked to programmed cell death pathways. We have analyzed several human breast cancer cell lines for the expression of bcl-2 and p53. We found an inverse correlation between the expression of the two proteins. The result suggested that mutant p53 could substitute for bcl-2 function in breast cancer cells and that could also down-regulate bcl-2 expression. We found, indeed, that overexpression of a mutant p53 (mut 175) in MCF-7 cells could induce down-regulation of bcl-2 both at protein and mRNA level. However, the promoter region of the human bcl-2 gene does not contain the negative regulatory element responsible for the down-regulation. If this mechanism will be proved also for the wild-type p53 allele, it may disclose a possible mechanism for p53-induced apoptosis: down-regulation of bcl-2.
1 This work was supported by the Council for Tobacco Research, USA, Grant 3496 to S. H. and National Cancer Institute Grant CA 39860 to C. M. C.
2 To whom requests for reprints should be addressed.
Received 2/ 3/94. Accepted 3/14/94.
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