Hepatitis B virus X protein-induced upregulation of CAT-1 stimulates proliferation and inhibits apoptosis in hepatocellular carcinoma cells.

// Rongjuan Dai 1, * , Feng Peng 1, * , Xinqiang Xiao 1 , Xing Gong 1 , Yongfang Jiang 1 , Min Zhang 1 , Yi Tian 1 , Yun Xu 1 , Jing Ma 1 , Mingming Li 1 , Yue Luo 1 and Guozhong Gong 1 1 Department of Infectious Diseases, Institute of Hepatology Central South University, Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, PR China * These authors contributed equally to this work and should be considered as co-first authors Correspondence to: Guozhong Gong, email: guozhonggong@yahoo.com Keywords: HBx, CAT-1, miR-122, Gld2, HCC Received: August 31, 2016      Accepted: April 23, 2017      Published: May 05, 2017 ABSTRACT The HBx protein of hepatitis B virus (HBV) is widely recognized to be a critical oncoprotein contributing to the development of HBV-related hepatocellular carcinoma (HCC). In addition, cationic amino acid transporter 1 (CAT-1) gene is a target of miR-122. In this study, we found that CAT-1 protein levels were higher in HBV-related HCC carcinomatous tissues than in para-cancerous tumor tissues, and that CAT-1 promoted HCC cell growth, proliferation, and metastasis. Moreover, HBx-induced decreases in Gld2 and miR-122 levels that contributed to the upregulation of CAT-1 in HCC. These results indicate that a Gld2/miR-122/CAT-1 pathway regulated by HBx likely participates in HBV-related hepatocellular carcinogenesis.