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Title: Promyelocytic leukemia protein is required for gain of function by mutant p53
Authors: Haupt, S.
Di Agostino, S.
Mizrahi, I.
Alsheich-Bartok, O.
Voorhoeve, M. 
Damalas, A.
Blandino, G.
Haupt, Y.
Issue Date: 1-Jun-2009
Citation: Haupt, S., Di Agostino, S., Mizrahi, I., Alsheich-Bartok, O., Voorhoeve, M., Damalas, A., Blandino, G., Haupt, Y. (2009-06-01). Promyelocytic leukemia protein is required for gain of function by mutant p53. Cancer Research 69 (11) : 4818-4826. ScholarBank@NUS Repository.
Abstract: Mutations in the p53 tumor suppressor are the most common genetic events in human cancer. These mutations not only result in a loss of wild-type p53 activity, but can also lead to a gain of new oncogenic properties. Understanding how these gained functions are regulated is in its infancy. In this study, we show that the promyelocytic leukemia (PML) protein is an important regulator of mutant p53. We show that PML interacts with mutant p53. Importantly, PML enhances the transcriptional activity of mutant p53. Unexpectedly, PML is required for the proliferation and colony formation of cancer cells bearing mutant p53. Down-regulation of PML expression inhibits the growth of mutant p53-expressing cancer cells, predominantly by promoting cell cycle arrest. Our results suggest that the tumor suppression function of PML depends on the status of p53. In the context of mutant p53, PML enhances its cancer-promoting activities. ©2009 American Association for Cancer Research.
Source Title: Cancer Research
ISSN: 00085472
DOI: 10.1158/0008-5472.CAN-08-4010
Appears in Collections:Staff Publications

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