Abstract:

Objective To explore the effects of sorafenib and inhibitors for mammalian target of rapamycine （mTOR） and PI3K on the proliferation and Ghrelin （GHRL） gene expression of hepatobiliary cancer cells.
MethodsThe invitro cultured human hepatocellular carcinoma SMMC7721 cells and bile ductcarcinoma QBC939 cells were treated with different concentrations（0, 50, 100, 200 μmol/L） of sorafenib， LY294002 （PI3K inhibitor） and Rapamycin （mTOR inhibitor） for 48 h. The proliferation rates of SMMC7721 and QBC939 cells were detected by MTS cell activity assay kit. The mRNA levels of GHRL were detected by quantitative realtime PCR （qPCR） in SMMC 7721 and QBC939 cells. Results Compared with the control group，there were decreased proliferative rates of SMMC7721 and QBC939 cells after the treatment with LY294002， sorafenib and Rapamycin in a dose-dependent manner （P＜0.05）. The qPCR results showed that there was no significant difference between the mRNA levels of GHRL in SMMC7721 cells treated with LY294002 and sorafenib in comparison with the control group （P＞0.05）. However， compared with the control group， the mRNA level of GHRL in the experimental group was increased with the elevated concentration of Rapamycin， and the difference was statistically significant（P＜0.05）. The mRNA levels of GHRL in QBC939 cells treated with LY294002，sorafenib and Rapamycin were higher than those in the control group with statistical significance（P＜0.05）. Conclusion Three agents can inhibit the proliferation of hepatobiliary cancer cells and promote the GHRL expression of QBC939 cells， but only Rapamycin can up regulate the expression of GHRL gene in SMMC7721 cells. The expression of GHRL gene is closely related to the occurrence of hepatocellular carcinoma and cholangiocarcinoma.