MiR-205 suppresses tumor growth, invasion, and epithelial-mesenchymal transition by targeting SEMA4C in hepatocellular carcinoma.

Growing evidence indicates that microRNAs are involved in tumorigenesis and progression of hepatocellular carcinoma (HCC). However, the functional mechanisms of miR-205 in HCC remain largely unknown. Here, we demonstrate that miR-205 expression was significantly down-regulated in HCC tissues and cell lines and was correlated with metastatic pathologic features and shorter disease-free and overall survival. Overexpression of miR-205 dramatically inhibited HCC cell proliferation, apoptosis, migration, invasion, epithelial-mesenchymal transition (EMT) in vitro, and tumor growth in vivo. We subsequently identified semaphorin 4C (SEMA4C) as a novel target of miR-205. Furthermore, high expression levels of SEMA4C were frequently found in HCC tissues and were associated with poor prognosis. Ectopic expression of SEMA4C restored the suppressive effect of overexpressed miR-205 on migration, invasion, and EMT. Taken together, our findings provide new insight into the critical role of miR-205 in regulating tumor growth, invasion, and EMT of HCC, suggesting miR-205 may serve as a promising therapeutic target and novel prognostic indicator for patients with HCC.-Lu, J., Lin, Y., Li, F., Ye, H., Zhou, R., Jin, Y., Li, B., Xiong, X., Cheng, N. MiR-205 suppresses tumor growth, invasion and epithelial-mesenchymal transition by targeting SEMA4C in hepatocellular carcinoma.