Fibroblast growth factor (FGF) 5 can inhibit the growth of hepatocellular cell line

Abstract

We completed the quantitative profiles of FGFs and FGFRs in hepatocellular carcinomas (HCC) and hepatoblastomas compared with normal liver cells in the previous study. Several FGFs including FGF5 and its functional receptors were hightly expressed in hepatocellular carcinoma cell lines even though the FGFs are not checked from normal liver cDNAs. As FGF5 are known to have the mitogenic and cell survival activity in the cancer, we studied to check the inhibition effect for hepatocellular carcinogenesis by interfering FGF5 activity with its siRNAs in the HCC cell lines. We knocked down the level of FGF5 using siRNA technology and measured the extent of cell proliferation and apoptosis in HepG2 cells. We checked the Erk1/2 activity in the FGF5 silencing cells comparing to that of control cell. We also investigated the addictive effect of FGF5 silencing on the cytotoxicity in the combination treatment of anti-cancer drug, Cisplatin. FGF5 silencing in HepG2 cell lines caused profound decrease the cell viability and Erk activation upon the serum stimulation. Cisplatin treatment in the FGF5 silencing cells showed dramatic increase the cytotoxicity resulting in the cellular apoptosis. These results showed that hapatocellular carcinogenesis may due to specific expression of several FGFs and its counterpart receptors. We also propose impairment of FGF5 function in the HCC may critical for liver cancer therapy.