Tensin2 with growth suppression and apoptosis induction activities is underexpressed in hepatocellular carcinoma

Abstract

Tensin is a family of focal adhesion proteins that strategically located among the extracellular matrix, actin cytoskeleton and signal transduction. Dysregulation of tensin members has been implicated in various human cancers. Accumulating evidence has shown that different members of tensin family are interacting partners of tumor suppressor, Deleted in liver cancer (DLC). Our recent study has identified tensin2 as the interacting partner of DLC1 and tensin2 itself exerted pronounced growth suppressive activity in hepatocellular carcinoma (HCC) cells. In the present study, we aimed to elucidate the role of tensin2 in hepatocarcinogenesis by determining the expression of tensin2 in human HCC tissues and ectopically expressing tensin2 in HCC cell line. Quantitative analysis of tensin2 expression revealed that it was underexpressed in 40% of human HCC. HCC cells stably expressing tensin2 displayed lower proliferation rate, decreased anchorage-independent growth, inhibited motility and invasiveness as compared with the vector transfectants. In addition, ectopic expression of tensin2 in HCC cells caused a dramatic suppression of colony formation and triggered apoptosis. The regulatory PTEN and SH2 domains were responsible for the biological activity of tensin2. In conclusion, our study showed that tensin2 was underexpressed in HCC and suggested the potential negative regulatory role of tensin2 in hepatocarcinogenesis.