Hepatitis B virus X protein-induced upregulation of CAT-1 stimulates proliferation and inhibits apoptosis in hepatocellular carcinoma cells
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Rongjuan Dai1,*, Feng Peng1,*, Xinqiang Xiao1, Xing Gong1, Yongfang Jiang1, Min Zhang1, Yi Tian1, Yun Xu1, Jing Ma1, Mingming Li1, Yue Luo1 and Guozhong Gong1
1Department 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
Guozhong Gong, email: [email protected]
Keywords: HBx, CAT-1, miR-122, Gld2, HCC
Received: August 31, 2016 Accepted: April 23, 2017 Published: May 05, 2017
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.
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