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Deleted in liver cancer-1 (DLC-1): a tumor suppressor not just for liver Liao YC; Lo SHInt J Biochem Cell Biol 2008[]; 40 (5): 843-7Deleted 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.|Animals[MESH]|Carcinoma, Hepatocellular/genetics[MESH]|GTPase-Activating Proteins[MESH]|Gene Expression Regulation[MESH]|Humans[MESH]|Liver Neoplasms/genetics[MESH]|Mice[MESH]|Neoplasms/diagnosis/drug therapy[MESH]|Protein Structure, Tertiary[MESH]|Rats[MESH]|Tumor Suppressor Proteins/chemistry/genetics/*physiology[MESH] |
