miR-454 functions as an oncogene by inhibiting CHD5 in hepatocellular carcinoma

Abstract

// Lei Yu 1, * , Xuejun Gong 2, * , Lei Sun 3 , Hong Yao 1 , Baoling Lu 1 , Liying Zhu 1 1 Department of Infectious Disease, The Fourth Hospital of Harbin Medical University, Harbin 150001, Heilongjiang, China 2 Department of Biliary and Pancreatic Surgery, Xiangya Hospital of Central South University, Changsha, 410008, Hunan, China 3 Department of Ophthalmology, The Fourth Hospital of Harbin Medical University, Harbin 150001, Heilongjiang, China * These authors contributed equally to this work Correspondence to: Li-Ying Zhu, e-mail: zlyhmu@126.com Lei Yu, e-mail: widedoor@sina.com Keywords: hepatocellular carcinoma, microRNA, miR-454, CHD5 Received: May 11, 2015      Accepted: July 17, 2015      Published: July 30, 2015 ABSTRACT Previous studies showed that miR-454 acted as an oncogene or tumor suppressor in cancer. However, its function in HCC remains unknown. In this study, we found that miR-454 expression was upregulated in HCC cell lines and tissues. Knockdown of miR-454 inhibited HCC cell proliferation and invasion and epithelial mesenchymal transition (EMT), whereas overexpression of miR-454 promoted HCC cell proliferation and invasion and EMT. Furthermore, we identified the CHD5 as a direct target of miR-454. CHD5 was downregulated in HCC tissues and cell lines and the expression level of CHD5 was inversely correlated with the expression of miR-454 in HCC tissues. In addition, knockdown of miR-454 inhibited the growth of HepG2-engrafted tumors in vivo . Taken together, these results indicated that miR-454 functioned as an oncogene in HCC.