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Upregulated long noncoding RNA PANDAR predicts an unfavorable prognosis and promotes tumorigenesis in cholangiocarcinoma

Authors Xu Y, Jiang X, Cui Y

Received 14 March 2017

Accepted for publication 6 May 2017

Published 6 June 2017 Volume 2017:10 Pages 2873—2883


Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Narasimha Reddy Parine

Peer reviewer comments 3

Editor who approved publication: Dr Samir Farghaly

Yi Xu,1,2 Xingming Jiang,1 Yunfu Cui1

1Department of Hepatopancreatobiliary Surgery, Second Affiliated Hospital of Harbin Medical University, 2The Key Laboratory of Myocardial Ischemia, Harbin Medical University, Ministry of Education, Harbin, People’s Republic of China

Abstract: Cholangiocarcinoma (CCA) is one of the most malignant human cancers with increasing incidence worldwide. LncRNAs have emerged as gene regulators and prognostic biomarkers in a variety of neoplasms. PANDAR, a novel cancer-related lncRNA, has been reported to be upregulated in diverse human carcinomas. In this study, we aimed to investigate the clinical significance of lncRNA PANDAR in CCA and explore its functional roles in CCA cells including cell proliferation, apoptosis, migration, invasion and epithelial-to-mesenchymal transition (EMT). The results showed that PANDAR was significantly upregulated in CCA ­tissue specimens and cell lines, and its high expression was closely associated with lymph node invasion (P=0.004), TNM stage (P=0.034) and postoperative relapse (P=0.006) in patients with CCA. Thus, overexpression of PANDAR could serve as an independent prognostic biomarker of CCA. Furthermore, silencing of PANDAR followed by siRNA significantly inhibited cell proliferation and increased apoptosis in CCA cells. In addition, suppression of PANDAR impaired migration and invasion capacity in vitro partly by affecting EMT. Overall, our findings showed that lncRNA PANDAR serves as a novel prognostic biomarker and therapeutic target for CCA.

Keywords: cholangiocarcinoma, lncRNA, PANDAR, prognosis, tumorigenesis

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