Downregulation of Talin1 promotes hepatocellular carcinoma progression through activation of the ERK1/2 pathway.

摘要: Talin1 is an adaptor protein that conjugates integrins to the cytoskeleton and regulates focal adhesion signaling. Several studies have found overexpressed in several tumor types promotes progression. However, explicit role of hepatocellular carcinoma (HCC) progression still unclear its functional mechanism remains largely unknown. In this study, we showed a trend gradually decreasing expression from normal liver tissues hepatocirrhosis, hyperplasia, corresponding adjacent non-tumor, primary HCC, eventually metastatic foci, indicating may correlate with HCC initiation was significantly downregulated compared non-tumor low associated poor prognosis. Furthermore, knockdown induced epithelial-mesenchymal transition promoted migration invasion SK-Hep-1 cells HepG2 cells. Mechanistically, ERK pathway responsible for these promoting effects The on transition, migration, were reversed by U0126, specific ERK1/2 inhibitor. Taken together, our results suggested might serve as suppressor potential prognostic biomarker patients.