FGF19 promotes epithelial-mesenchymal transition in hepatocellular carcinoma cells by modulating the GSK3β/β- catenin signaling cascade via FGFR4 activation

摘要: Compelling evidence suggests that the epithelial-mesenchymal transition (EMT) correlates with aggressiveness of tumors and poor survival. FGF19 has been shown to be involved in EMT cholangiocarcinoma colorectal cancer, however, molecular mechanisms underlying FGF19-induced process hepatocellular carcinoma (HCC) remain largely unknown. Here, we show expression is significantly elevated negatively associated E-cadherin HCC tissues cell lines. Ectopic promotes invasion epithelial-like cells through repression expression, whereas knockdown enhances hence diminishes traits mesenchymal-like cells, suggesting exerts its tumor progressing functions as an inducer. Interestingly, depletion cannot abrogate presence GSK3β inhibitors. Furthermore, can markedly attenuated when FGFR4 knocked out. These observations clearly indicate FGFR4/GSK3β/β-catenin axis may play a pivotal role cells. As specific receptor are frequently amplified selective targeting this signaling node lend insights into potential effective therapeutic approach for blocking metastasis HCC.