Research Papers:

This article is currently undergoing investigation.

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

Congren Wang _, Xuejin Wang, Zijian Su, Hongjiang Fei, Xiaoyu Liu and Qunxiong Pan

PDF  |  HTML  |  Supplementary Files  |  How to cite  |  Order a Reprint

Oncotarget. 2015; 6:36231-36244. https://doi.org/10.18632/oncotarget.4740

Metrics: PDF 1602 views  |   HTML 1264 views  |   ?  


Congren Wang1, Xuejin Wang2, Zijian Su1, Hongjiang Fei1, Xiaoyu Liu1, Qunxiong Pan1

1Department of Surgical Oncology, First Hospital of Quanzhou Affiliated to Fujian Medical University, Quanzhou 362000, China

2Department 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


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.

Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.
PII: 4740