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Int J Biochem Cell Biol. 2008;40(5):843-7. Epub 2007 Apr 20.

Deleted in liver cancer-1 (DLC-1): a tumor suppressor not just for liver.

Author information

1
Lawrence Ellison Center for Tissue Regeneration and Repair, Department of Biochemistry and Molecular Medicine, University of California, Davis, Sacramento, CA 95817, USA.

Abstract

Deleted in liver cancer 1 (DLC-1), as its name implied, was originally isolated as a potential tumor suppressor gene often deleted in hepatocellular carcinoma. Further studies have indicated that down-expression of DLC-1 either by genomic deletion or DNA methylation is associated with a variety of cancer types including lung, breast, prostate, kidney, colon, uterus, ovary, and stomach. Re-expression of DLC-1 in cancer cells regulates the structure of actin cytoskeleton and focal adhesions and significantly inhibits cell growth, supporting its role as a tumor suppressor. This tumor suppressive function relies on DLC-1's RhoGTPase activating protein (RhoGAP) activity and steroidogenic acute regulatory (StAR)-related lipid transfer (START) domain, as well as its focal adhesion localization, which is recruited by the Src Homology 2 (SH2) domains of tensins in a phosphotyrosine-independent fashion. Therefore, the expression and subcellular localization of DLC-1 could be a useful molecular marker for cancer prognosis, whereas DLC-1 and its downstream signaling molecules might be therapeutic targets for the treatment of cancer.

PMID:
17521951
PMCID:
PMC2323245
DOI:
10.1016/j.biocel.2007.04.008
[Indexed for MEDLINE]
Free PMC Article

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