Carbonic anhydrase III promotes transformation and invasion capability in hepatoma cells through FAK signaling pathway
Journal
Molecular Carcinogenesis
Journal Volume
47
Journal Issue
12
Pages
956-963
Date Issued
2008
Author(s)
Abstract
Carbonic anhydrase III (CAIII) is distinguished from the other members of the CA family by low carbon dioxide hydratase activity, resistance to the CA inhibitor acetazolamide, and a predominant expression in the liver of males. In this report the effects of CAIII expression on liver cancer cells invasiveness were explored. Overexpression of CAIII in the HCC cell line SK-Hep1 resulted in increased anchorage-independent growth and invasiveness. And siRNA-mediated silencing of CAIII expression decreased the invasive ability of SK-Hep1 cells. Furthermore, CAIII transfectants showed elevated focal adhesion kinase (FAK) and Src activity. Silencing of FAK expression in CAIII transfectants led to suppression of HCC cell invasion. More importantly, the CAIII transfectants acidified the culture medium at an accelerated speed than the control cells did. Taken together, these data suggest that the CAIII-promoted invasive ability of HCC cells may probably be mediated through, at least in part, the FAK signaling pathway via intracellular and/or extracellular acidification.
Other Subjects
carbonate dehydratase III; focal adhesion kinase; small interfering RNA; article; cancer cell culture; cell culture; cell growth; cell invasion; cell transformation; controlled study; culture medium; genetic transfection; hepatoma cell; human; human cell; liver cell carcinoma; priority journal; Carbonic Anhydrase III; Carcinoma, Hepatocellular; Cell Line, Tumor; Cell Transformation, Neoplastic; Focal Adhesion Protein-Tyrosine Kinases; Humans; Liver Neoplasms; Male; Neoplasm Invasiveness; Signal Transduction
Type
journal article