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

Yi Chun Liao, Su Hao Lo

Research output: Contribution to journalArticle

85 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)843-847
Number of pages5
JournalInternational Journal of Biochemistry and Cell Biology
Volume40
Issue number5
DOIs
StatePublished - 2008

Fingerprint

Liver Neoplasms
Liver
Tumors
Neoplasms
Focal Adhesions
Adhesion
Phosphotyrosine
src Homology Domains
Cell growth
DNA Methylation
Tumor Suppressor Genes
Actin Cytoskeleton
Uterus
Names
Actins
Prostate
Hepatocellular Carcinoma
Ovary
Lung Neoplasms
Stomach

Keywords

  • DLC
  • Focal adhesion
  • Tumor suppressor

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology

Cite this

Deleted in liver cancer-1 (DLC-1) : A tumor suppressor not just for liver. / Liao, Yi Chun; Lo, Su Hao.

In: International Journal of Biochemistry and Cell Biology, Vol. 40, No. 5, 2008, p. 843-847.

Research output: Contribution to journalArticle

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