Background/aims: The fragile histidine triad (FHIT) gene is a candidate tumor suppressor gene. Recent studies have found that FHIT protein is lost in digestive system neoplasms. However, there is limited information on the effect of FHIT on apoptosis and the regulation functions on cyclin D1 in cholangiocarcinoma.
Methodology: Eukaryotic expression plasmids with/without the FHIT gene were constructed and transfected into three groups in which cholangiocarcinoma cells were also divided. We observed the proliferation of cholangiocarcinoma by using the MTT method and flow cyclometry (FCM). Invasive ability was then determined via transwell chamber testing. In addition, to examine whether FHIT mRNA and protein expression were correlated with cyclin D1 expression, we used real-time RT-PCR and western blotting.
Results: The absorbance (A490) was decreased significantly (p<0.05) according to MTT, showing that proliferation had been inhibited and the apoptosis ratio after transfecting had increased significantly (p<0.05). The amount of cells which passed the filter in the transwell chamber was significantly less (p<0.05). The expression of cyclin D1 mRNA and the protein was decreased from the original cell line (p<0.05).
Conclusions: The results suggest that increased FHIT gene activity can promote apoptosis of cholangiocarcinoma and reduce the expression level of cyclin D1.