Liao, Y.-C.Y.-C.LiaoLo, S.H.S.H.LoYI-CHUN LIAO2018-09-102018-09-10200813572725http://www.scopus.com/inward/record.url?eid=2-s2.0-40149083557&partnerID=MN8TOARShttp://scholars.lib.ntu.edu.tw/handle/123456789/340325https://www.scopus.com/inward/record.uri?eid=2-s2.0-40149083557&doi=10.1016%2fj.biocel.2007.04.008&partnerID=40&md5=df9c754e6d4e46728cbfbb039313500fDeleted 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. © 2007 Elsevier Ltd. All rights reserved.DLC; Focal adhesion; Tumor suppressor[SDGs]SDG3short survey10.1016/j.biocel.2007.04.008175219512-s2.0-40149083557