miR-25 promotes hepatocellular carcinoma cell growth, migration and invasion by inhibiting RhoGDI1

Abstract

// Congren Wang 1 , Xuejin Wang 2 , Zijian Su 1 , Hongjiang Fei 1 , Xiaoyu Liu 1 , Qunxiong Pan 1 1 Department of Surgical Oncology, First Hospital of Quanzhou Affiliated to Fujian Medical University, Quanzhou 362000, China 2 Department of Obstetrics and Gynecology, Second Affiliated Hospital of Fujian Medical University, Quanzhou 362000, China Correspondence to: Qunxiong Pan, e-mail: qxpan1@163.com Keywords: miR-25, hepatocellular carcinoma, RhoGDI1, metastasis Received: February 25, 2015      Accepted: September 26, 2015      Published: October 10, 2015 ABSTRACT MicroRNA (miRNA)-25 is a small non-coding RNA that has been implicated in the tumorigenesis of many cancers, but little is known on the role of miR-25 in HCC metastasis. We hereby found that miR-25 was significantly upregulated in clinical HCC tissues compared with normal liver tissues. We also revealed that miR-25 dramatically stimulates HCC cell growth and activates the epithelial-mesenchymal transition (EMT). MiR-25 is activated by the WNT/β-catenin signaling pathway, and exerts its pro-metastatic function by directly inhibiting the Rho GDP dissociation inhibitor alpha (RhoGDI1). Downregulation of RhoGDI1 enhances expression of Snail, thereby promoting EMT. MiR-25 levels are positively correlated with β-catenin expression, whereas negatively correlated with the level of RhoGDI1 in HCC. Our findings provide new insights into the role of miR-25 in HCC metastasis, and implicate the potential application of miR-25 in HCC therapy.