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A more recent version of this article appeared on February 1, 2007.
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Submitted on August 10, 2006
Revised on October 30, 2006
Accepted on November 16, 2006

Up-regulation of tumor susceptibility gene 101 protein in ovarian carcinomas revealed by proteomic analyses

Travis W. Young, Fang C. Mei, Daniel G. Rosen, Gong Yang, Nan Li, Jinsong Liu, and Xiaodong Cheng

Pharmacology and Toxicology, The University of Texas Medical Branch, Galveston, TX 77555-1031

Corresponding Author: xcheng{at}utmb.edu

Small GTPase RAS plays a critical role in cellular signaling and oncogenic transformation. Proteomic analysis of genetically-defined human ovarian cancer models identified the tumor susceptibility gene 101 (TSG101) as a down stream target of RAS oncogene. Mechanistic studies revealed a novel post-translational regulation of TSG101 through the RAS/RAF/MEK/MAPK signaling pathway and down-stream molecules p14ARF/HDM2. Immuno-analysis using ovarian cancer samples and micro-tissue array revealed elevated TSG101 levels in human ovarian carcinomas. Silencing of TSG101 by siRNA in ovarian cancer cells led to growth inhibition and cell death. Concurrent with the apparent growth inhibitory effect, the levels of the CBP/p300-interacting transactivator with ED-rich tail 2 (CITED2) and hypoxia inducible factor 1a (HIF-1a), as well as its cellular activity, were markedly reduced after TSG101 knockdown. These results demonstrate that TSG101 is important for CITED2 and HIF-1a mediated cellular regulation in ovarian carcinomas.


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Home page
 Mol. Biol. CellHome page
B. McDonald and J. Martin-Serrano
Regulation of Tsg101 Expression by the Steadiness Box: A Role of Tsg101-associated Ligase
Mol. Biol. Cell, February 1, 2008; 19(2): 754 - 763.
[Abstract] [Full Text] [PDF]

Home page
 Clin. Cancer Res.Home page
T. W. Young, D. G. Rosen, F. C. Mei, N. Li, J. Liu, X.-F. Wang, and X. Cheng
Up-regulation of Tumor Susceptibility Gene 101 Conveys Poor Prognosis through Suppression of p21 Expression in Ovarian Cancer
Clin. Cancer Res., July 1, 2007; 13(13): 3848 - 3854.
[Abstract] [Full Text] [PDF]


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