Research Papers:

Long non-coding RNA00364 represses hepatocellular carcinoma cell proliferation via modulating p-STAT3-IFIT2 signaling axis

Wei-Guo Tang, Bo Hu, Hai-Xiang Sun, Qi-Man Sun, Chao Sun, Pei-Yao Fu, Zhang-Fu Yang, Xin Zhang, Chen-Hao Zhou, Jia Fan, Ning Ren and Yang Xu _

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Oncotarget. 2017; 8:102006-102019. https://doi.org/10.18632/oncotarget.22039

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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

Correspondence to:

Yang Xu, email: [email protected]

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.

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