摘要

Accumulating evidence indicates that microRNAs (miRNAs) play important roles in tumorigenesis and metastasis. Recent research has shown that miR-196b is implicated in metastasis by regulating the migration and invasion of cancer cells. However, the clinical significance of miR-196b and its role as well as the underlying mechanisms in hepatocellular carcinoma (HCC) remain largely unknown. Here, we detected miR-196b expression in HCC and matched non-tumor tissues with qRT-PCR. We found that miR-196b displayed higher expression in HCC patient tissues and cells. Clinical analysis revealed that high miR-196 expression was correlated with venous infiltration, advanced TNM stage and poor prognosis. Functionally, we demonstrated that miR-196b promoted the migration and invasion of HCC cells in vitro. Moreover, miR-196b knockdown restrained pulmonary metastasis in vivo. Mechanistically, we confirmed that miR-196b could directly bind to 3'UTR of forkhead box P2 (FOXP2) mRNA and repress its expression. miR-196b and FOXP2 showed a negative correlation in HCC tissues. More importantly, upregulation of FOXP2 antagonized miR-196b-mediated migration and invasion in Hep3B cells. Furthermore, FOXP2 knockdown partially reversed the anti-metastatic function of the miR-196b inhibitor on HCCLM3 cells. Taken together, we demonstrated that miR-196b may function as a prognostic biomarker and suppressed FOXP2 expression, subsequently leading to the metastasis of HCC. Our findings highlight a novel mechanism of miR-196b in the progression of HCC and identify miR-196b/FOXP2 axis as a promising target for HCC.