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

Congren Wang; Xuejin Wang; Zijian Su; Hongjiang Fei; Xiaoyu Liu; Qunxiong Pan

doi:10.18632/oncotarget.4740

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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

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

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Abstract

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: [email protected]

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.

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

Abstract