Research Papers:
Long noncoding RNA XIST promotes malignancies of esophageal squamous cell carcinoma via regulation of miR-101/EZH2
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Abstract
Xiaoliang Wu1,2,*, Xiaoxiao Dinglin3,*, Xing Wang2,*, Wen Luo1, Qi Shen1, Yong Li1, Ling Gu2,4, Qianghua Zhou2, Haotu Zhu2, Yanjie Li5, Chaodi Tan6, Xianzi Yang7 and Zhenfeng Zhang8,2
1Department of Oncology, Guizhou Provincial People’s Hospital, Guiyang, China
2State Key Laboratory of Oncology in South China & Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China
3Department of Medical Oncology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China
4Puer University, Puer, China
5The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China
6Sun Yat-sen University, Guangzhou, China
7Affiliated Cancer Hospital & Institute of Guangzhou Medical University, Guangzhou, China
8Department of Radiology, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, China
*These authors have contributed equally to this work
Correspondence to:
Zhenfeng Zhang, email: [email protected]
Xianzi Yang, email: [email protected]
Keywords: long non-coding RNA, XIST, EZH2, esophageal squamous cell carcinoma, EMT
Received: March 08, 2017 Accepted: May 22, 2017 Published: June 27, 2017
ABSTRACT
The long non-coding RNA XIST is a long non-coding RNA that associates with polycomb repressive complex 2 to regulate X-chromosome inactivation in female mammals. The biological roles as well as the underlying mechanisms of XIST in esophageal squamous cell carcinoma remained yet to be solved. Our data indicated that XIST was significantly upregulated in esophageal squamous cancerous tissues and cancer cell lines, as compared with that in the corresponding non-cancerous tissues and immortalized normal squamous epithelial cells. High XIST expression predicted poor prognosis of esophageal squamous cancer patients. Lentivirus mediated knockdown of XIST inhibited proliferation, migration and invasion of esophageal squamous cancer cells in vitro and suppressed tumor growth in vivo. Knockdown of XIST resulted in elevated expression of miR-101 and decreased expression of EZH2. Further analysis showed that XIST functioned as the competitive endogenous RNA of miR-101 to regulate EZH2 expression. Moreover, enforced expression of EZH2 significantly attenuated the anti-proliferation activity upon XIST knockdown. Conclusively, XIST plays an important role in malignant progression of ESCC via modulation of miR-101/EZH2 axis.
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