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J. Biol. Chem., Vol. 276, Issue 9, 6874-6878, March 2, 2001
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From the MDM2 is a short-lived protein that regulates p53
degradation. We report here that transient coexpression of MDM2 and
several p53 hotspot mutants resulted in stabilization and
increased expression of MDM2. Ectopic expression of the mutant
p53175H allele by recombinant adenovirus
infection or stable transfection also stabilized endogenous MDM2 in
p53-null cells. A panel of human tumor cell lines
expressing different endogenous mutant p53 alleles also contained
stabilized nuclear MDM2 at elevated levels when compared with
p53-null cells. MDM2 was present in complexes with mutant
p53 in tumor cells, and stabilization of MDM2 required direct binding
to mutant p53. These results reveal a novel property of mutant p53 and
a unique feature of tumors with p53 missense mutations.
Accumulation of stable MDM2 may contribute to tumorigenesis
through its p53-independent transforming functions.
Stabilization of the MDM2 Oncoprotein by Mutant p53*
,,,,¶
Molecular Oncology Program, H. Lee Moffitt
Cancer Center and Research Institute, Tampa, Florida 33612 and
§ Hybridon, Inc., Cambridge, Massachusetts 02139
*
This work was supported by the H. Lee Moffitt Cancer Center
and by grants from the National Institutes of Health and the American Cancer Society (to J. C.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
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