Long non-coding RNA00364 represses hepatocellular carcinoma cell proliferation via modulating p-STAT3-IFIT2 signaling axis
Metrics: PDF 861 views | HTML 1314 views | ?
Wei-Guo Tang1,2,3,*, Bo Hu1,*, Hai-Xiang Sun1,*, Qi-Man Sun1, Chao Sun1, Pei-Yao Fu1, Zhang-Fu Yang1, Xin Zhang1, Chen-Hao Zhou1, Jia Fan1, Ning Ren1,2,3 and Yang Xu1
1Department of Liver Surgery, Liver Cancer Institute, Zhongshan Hospital, Fudan University; Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Shanghai 200032, P. R. China
2Department of Surgery, Minhang Branch of Zhongshan Hospital, Fudan University, Shanghai 201199, P. R. China
3Institute of Fudan-Minhang Academic Health System, Minhang Hospital, Fudan University, Shanghai 201199, P. R. China
*These authors have contributed equally to this work
Yang Xu, email: email@example.com
Keywords: hepatocellular carcinoma; long noncoding RNA00364; interferon-γ; p-STAT3/IFIT2; prognosis
Received: December 19, 2016 Accepted: August 28, 2017 Published: October 25, 2017
The effects of long non-coding RNAs (lncRNAs) on hepatocellular carcinoma (HCC) remain largely unclear. In this study, we identified an interferon (IFN)-γ-induced LncRNA, LncRNA00364, in HCC by microarray. LncRNA00364 displays lower expression in HCC tumor samples compared to paired normal controls. Overexpression of LncRNA00364 inhibits cell proliferation, G1/S cell cycle progression and promotes apoptosis in HCC cell lines. Consistently, LncRNA00364 overexpression leads to decreased HCC tumor formation in vivo. Mechanistically, LncRNA00364 specifically binds with STAT3, resulting in inhibition of STAT3 phosphorylation and therefore leads to upregulation of IFIT2. In a clinical setting, LncRNA00364 shows an independent prognostic indicator for overall survival and cumulative recurrence in HCC patients, and correlates with IFIT2. Therefore, our study provides new insights into a novel therapeutic avenue targeting the LncRNA00364 signaling axis in HCC.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.