TGF-β1 Promotes Hepatocellular Carcinoma Invasion and Metastasis via ERK Pathway-Mediated FGFR4 Expression

作者：Jiawei Huang, Mengyuan Qiu, Li Wan, Gui Wang, Tongzhou Huang, Zhixin Chen, Songmin Jiang, Xiaokun Li, Lixiao Xie, Lin Cai · 发表于：Cellular Physiology and Biochemistry · 年份：2018 · DOI：10.1159/000487737 · 被引用次数：36 · 研究领域：Fibroblast Growth Factor Research、Liver physiology and pathology、Angiogenesis and VEGF in Cancer

BACKGROUND/AIMS: TGF-β1 is beneficial during early liver disease but is tumor-progressive during late stages especially for hepatocellular carcinoma (HCC). Thus, exploring the underlying mechanisms may provide information about a potentially therapeutic role of TGF-β1 in HCC. METHODS: Western blot and real-time quantitative PCR were used to quantify FGFR4 expression in HCC cell lines and a normal liver cell line. After constructing the best silencing FGFR4 expression vector, migration and invasiveness of TGF-β1 in HCC was studied in vitro and in vivo. Western blot was used to study the mechanism of TGF-β1 induction on FGFR4 expression with various inhibitors. RESULTS: HepG2 cell lines had the most FGFR4 expression, and data show that silencing FGFR4 suppressed cell proliferation, invasion and migration in HCC induced by TGF-β1 in vitro and in vivo. Moreover, TGF-β1 induced FGFR4 expression through the ERK pathway. CONCLUSION: Promoting FGFR4 expression via the ERK pathway, TGF-β1 contributes to HCC invasion and metastasis.