Long non-coding RNA FEZF1-AS1 promotes cell invasion and epithelial-mesenchymal transition through JAK2/STAT3 signaling pathway in human hepatocellular carcinoma

被引:34
|
作者
Wang, Ya-Dong [1 ,2 ]
Sun, Xue-Jun [1 ]
Yin, Jia-Jun [2 ]
Yin, Min [2 ]
Wang, Wei [2 ]
Nie, Zhe-Qun [2 ]
Xu, Jian [2 ]
机构
[1] Xi An Jiao Tong Univ, Dept Gen Surg, Affiliated Hosp 1, 277 West Yanta Rd, Xian 710061, Shaanxi, Peoples R China
[2] Dalian Univ, Affiliated Zhongshan Hosp, Dept Gen Surg, Dalian 116001, Peoples R China
关键词
FEZF1-AS1; Hepatocellular carcinoma; Cell cycle; Epithelial-mesenchymal transition; JAK2/STAT3 signaling pathway; PROLIFERATION; CANCER; MIGRATION;
D O I
10.1016/j.biopha.2018.05.116
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Long non-coding RNAs (lncRNAs) have emerged as key regulators in the development of hepatocellular carcinoma (HCC). In the present study, we explored the expression profile and biological role of lncRNA FEZF1-AS1 in HCC. We observed remarkable upregulation of FEZF1-AS1 in HCC tissues and cell lines, and high FEZF1-AS1 expression was correlated with aggressive phenotypes and poor prognosis of HCC patients. Furthermore, we found that FEZF1-AS1 knockdown markedly inhibited the proliferation of HCC cells by inducing cell cycle arrest. In addition, FEZF1-AS1 knockdown suppressed HCC tumor growth in vivo. Moreover, FEZF1-AS1 knockdown inhibited the migration and invasion of HCC cells through suppression of JAK2/STAT3 signaling-mediated epithelial-mesenchymal transition (EMT). In conclusion, the present study for the first time demonstrated that FEZF1-AS1 serves as an oncogenic lncRNA in human HCC and implicated FEZF1-AS1 as a valuable therapeutic target for HCC treatment.
引用
收藏
页码:134 / 141
页数:8
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