Non-coding RNA LINC00857 is predictive of poor patient survival and promotes tumor progression via cell cycle regulation in lung cancer
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Lihui Wang1,2, Yanli He2,3, Weijun Liu2,4, Shengbin Bai2,5, Lei Xiao2,5, Jie Zhang2,6, Saravana M. Dhanasekaran7, Zhuwen Wang2, Shanker Kalyana-Sundaram7, O. Alejandro Balbin7, Sudhanshu Shukla7, Yi Lu1, Jules Lin2, Rishindra M. Reddy2, Philip W. Carrott, Jr.2, William R. Lynch2, Andrew C. Chang2, Arul M. Chinnaiyan7, David G. Beer2, Jian Zhang1, Guoan Chen2
1Guangxi Medical University, Nanning, China
2Section of Thoracic Surgery, Department of Surgery, University of Michigan, Ann Arbor, Michigan, United States of America
3Guangzhou University of Chinese Medicine, Guangzhou, China
4The First People‘s Hospital of Yunnan Province, Kunming, China
5Xinjiang Medical University, Xinjiang, China
6Xi’an Jiaotong University, Xi’an, China
7Department of Pathology, University of Michigan, Ann Arbor, Michigan, United States of America
David G. Beer, e-mail: firstname.lastname@example.org
Jian Zhang, e-mail: email@example.com
Guoan Chen, e-mail: firstname.lastname@example.org
Keywords: non-coding RNA, LINC00857, lung adenocarcinoma, prognosis, diagnosis
Received: October 15, 2015 Accepted: January 24, 2016 Published: February 05, 2016
We employed next generation RNA sequencing analysis to reveal dysregulated long non-coding RNAs (lncRNAs) in lung cancer utilizing 461 lung adenocarcinomas (LUAD) and 156 normal lung tissues from 3 separate institutions. We identified 281 lncRNAs with significant differential-expression between LUAD and normal lung tissue. LINC00857, a top deregulated lncRNAs, was overexpressed in tumors and significantly associated with poor survival in LUAD. knockdown of LINC00857 with siRNAs decreased tumor cell proliferation, colony formation, migration and invasion in vitro, as well as tumor growth in vivo. Overexpression of LINC00857 increased cancer cell proliferation, colony formation and invasion. Mechanistic analyses indicated that LINC00857 mediates tumor progression via cell cycle regulation. Our study highlights the diagnostic/prognostic potential of LINC00857 in LUAD besides delineating the functional and mechanistic aspects of its aberrant disease specific expression and potentially using as a new therapeutic target.
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