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1 Department of Biochemistry and the Massey Cancer Center, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA
Requests for reprints: Swati Palit Deb, Department of Biochemistry, Sanger Hall, Virginia Commonwealth University, 1101 East Marshall Street, Richmond, VA 23298. Phone: (804) 828-9541; Fax: (804) 827-1427. E-mail: spdeb{at}hsc.vcu.edu
Abstract
The protein (MDM2) coded by the mouse double minute-2 (mdm2) gene or its human homologue is well known as an oncoprotein. Malignant human tumors particularly breast tumors and soft tissue sarcomas frequently overexpress MDM2. Artificial amplification of mdm2 gene derived from a transformed murine cell line enhances tumorigenic potential of murine cells. Consistent with its tumorigenic property, mouse or human MDM2 can inactivate several functions of the tumor suppressor p53 and can degrade p53. The protein also interacts with other tumor suppressors, and these interactions may contribute to its tumorigenic property. In spite of its oncogenic role, mouse or human MDM2 induces G1 arrest in normal human or murine cells. Some cell lines bearing known genetic mutations are insensitive to MDM2-mediated growth arrest. This review is aimed to collect available information on the functions of MDM2 that could potentially regulate cell cycle and to discuss how this information may fit in one model that could explain the two apparently opposite G1 arrest and oncogenic function of MDM2.
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