miR-454 functions as an oncogene by inhibiting CHD5 in hepatocellular carcinoma
Metrics: PDF 883 views | HTML 1141 views | ?
Lei Yu1,*, Xuejun Gong2,*, Lei Sun3, Hong Yao1, Baoling Lu1, Liying Zhu1
1Department of Infectious Disease, The Fourth Hospital of Harbin Medical University, Harbin 150001, Heilongjiang, China
2Department of Biliary and Pancreatic Surgery, Xiangya Hospital of Central South University, Changsha, 410008, Hunan, China
3Department of Ophthalmology, The Fourth Hospital of Harbin Medical University, Harbin 150001, Heilongjiang, China
*These authors contributed equally to this work
Li-Ying Zhu, e-mail: firstname.lastname@example.org
Lei Yu, e-mail: email@example.com
Keywords: hepatocellular carcinoma, microRNA, miR-454, CHD5
Received: May 11, 2015 Accepted: July 17, 2015 Published: July 30, 2015
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.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.