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LINC00963 Promotes Ovarian Cancer Proliferation, Migration and EMT via the miR-378g /CHI3L1 Axis

Authors Liu W, Yang YJ, An Q

Received 29 August 2019

Accepted for publication 21 November 2019

Published 21 January 2020 Volume 2020:12 Pages 463—473


Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Dr Sanjeev Srivastava

Wei Liu, Yu-Jia Yang, Qiang An

Department of Gynecology, Affiliated Hospital of Zunyi Medical University, Zunyi, Guizhou, People’s Republic of China

Correspondence: Yu-Jia Yang
Department of Gynecology, Affiliated Hospital of Zunyi Medical University, 149 Dalian Road, Zunyi City, Guizhou Province 563003, People’s Republic of China
Tel +86 13985608599

Background: Long non-coding RNA (lncRNAs) are involved in the development and progression of numerous tumors. Nevertheless, their role in ovarian cancer (OC) needs further study.
Methods: A pivotal lncRNA that modulated OC to metastasize was determined in this research, and its potential mechanism was inquired by qRT-PCR, CCK-8, EdU, Transwell assay, wound healing assay and Western blot assay.
Results: In our study, the GSE119054 microarray was analyzed, and LINC00963 showed a significant higher level in ovarian cancer tissues compared with controls. So LINC00963 was selected as research object. It was discovered that LINC00963 displayed a close relationship with unfavorable prognosis, and it was prominently raised in OC tissues of patients with lymph node metastasis. What’s more, LINC00963 downregulation in OC cells inhibited cell migration and invasion and inverted EMT triggered by TGF-β 1. LINC00963 downregulation also inhibited tumorigenesis in nude mice. In addition, results show that LINC00963 is a cytoplasmic lncRNA that shares the miRNA response elements (MREs) of miR-378g with CHI3L1, which is confirmed by a luciferase reporter assay and AGO2-dependent RNA immunoprecipitation (RIP).
Conclusion: On the whole, our results demonstrate an explicit oncogenic role of LINC00963 in ovarian cancer tumorigenesis via competition with miR-378g, suggesting a new regulatory mechanism of LINC00963 and providing a potential therapeutic target for ovarian cancer patients.

Keywords: ovarian cancer, migration, miR-378g, CHI3L1, LINC00963

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