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LncRNA PVT1 promotes proliferation, invasion and epithelial–mesenchymal transition of renal cell carcinoma cells through downregulation of miR-16-5p

Authors Ren Y, Huang W, Weng G, Cui P, Liang H, Li Y

Received 9 October 2018

Accepted for publication 7 February 2019

Published 5 April 2019 Volume 2019:12 Pages 2563—2575


Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Narasimha Reddy Parine

Peer reviewer comments 2

Editor who approved publication: Dr Sanjeev Srivastava

Yu Ren,1 Weiping Huang,2 Guobin Weng,1 Pinger Cui,1 Haote Liang,2 Yeping Li2

1Department of Urology, Ningbo Urology and Nephrology Hospital, Ningbo 315000, Zhejiang Province, People’s Republic of China; 2Department of Urology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, Zhejiang Province, People’s Republic of China

Background: LncRNAs have recently emerged as vital regulators in the pathogenesis and development of various cancers. LncRNA PVT1 is reported to function as an oncogene in some tumors. However, the role of PVT1 in RCC remains unknown.
Purpose: To explore the potential effects of lncPVT1 on the development of renal cell carcinoma.
Methods: The expression of PVT1 in renal cancer cell lines and tissues was measured by qRT-PCR. The endogenous PVT1 was silenced by RNAi. Cell viabilities were measured by the MTT assay. The migration and invasion of cells were investigated by the transwell assay. The apoptosis of cells was measured by the Nucleosome ELISA and caspase-3 activity assays. The levels of proteins were measured by the western blot.
Results: We found that PVT1 was upregulated in RCC tissues compared with the adjacent normal tissues. PVT1 expression was closely correlated with TNM stage, Fuhrman grade, lymph node metastasis and tumor size. Kaplan–Meier analysis revealed that high expression of PVT1 was significantly associated with poor overall survival. In accordance, overexpression of PVT1 was observed in RCC cells comto HK-2 cell. Silencing of PVT1 significantly repressed cell viability, induced apoptosis and inhibited cell migration and invasion in vitro. Furthermore, bioinformatic analysis and luciferase reporter assay confirmed that miR-16-5p was a target of PVT1. Silencing of miR-16-5p mostly reversed the regulatory effects on RCC cells induced by downregulation of PVT1.
Conclusion: In summary, our study indicates that targeting PVT1 might represent a rational therapeutic strategy for RCC.

Keywords: renal carcinoma, PVT1, migration, invasion, apoptosis, miR-16-5p
Corrigendum for this paper has been published


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