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MiR-34a Inhibits Cell Proliferation and Induces Apoptosis in Human Nasopharyngeal Carcinoma by Targeting lncRNA MCM3AP-AS1

Authors Sun P, Feng Y, Guo H, Li R, Yu P, Zhou X, Pan Z, Liang Y, Yu B, Zheng Y, Shi Y, Wen L, Wei M, Chen Y

Received 10 January 2020

Accepted for publication 26 May 2020

Published 22 June 2020 Volume 2020:12 Pages 4799—4806

DOI https://doi.org/10.2147/CMAR.S245520

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Antonella D'Anneo


Piyun Sun, Yuchen Feng, Hui Guo, Rong Li, Peng Yu, Xingguang Zhou, Zhige Pan, Yanyan Liang, Bihan Yu, Yanyi Zheng, Yu Shi, Lingbo Wen, Minmei Wei, Yanhua Chen

Department of Oncology, Liuzhou Hospital of Traditional Chinese Medicine, Liuzhou City, Guangxi Province 545001, People’s Republic of China

Correspondence: Yanhua Chen Tel +86 772-3357233
Email rp0571@163.com

Introduction: MCM3AP-AS1 has been characterized as an oncogenic lncRNA in several types of cancer, while its role in nasopharyngeal carcinoma (NPC) is unknown. This study aimed to investigate the role of MCM3AP-AS1 in NPC.
Patients and Methods: Paired NPC tissues and non-tumor tissues were collected from 55 NPC patients. Expression of MCM3AP-AS1 and miR-34a in paired tissues was analyzed by RT-qPCR. Interactions between MCM3AP-AS1 and miR-34a were analyzed by overexpression experiments. The roles of MCM3AP-AS1 and miR-34a in regulating NPC cell proliferation and apoptosis were explored by cell proliferation assay and cell apoptosis assay, respectively.
Results: Our bioinformatics analysis showed that MCM3AP-AS1 may be targeted by miR-34a, which is a well-studied tumor suppressor miRNA. In this study, we showed that miR-34a was downregulated and MCM3AP-AS1 was upregulated in NPC. An inverse correlation between the expression of MCM3AP-AS1 and miR-34a was found across NPC tissue samples. High expression level of MCM3AP-AS1 and low levels of miR-34a in NPC tissues predicted the poor survival. In NPC cells, overexpression of MCM3AP-AS1 did not affect the expression of miR34a, while overexpression of miR-34a led to downregulated MCM3AP-AS1. Cell proliferation and apoptosis assay showed that overexpression of miR-34a reduced the enhancing effects of overexpressing MCM3AP-AS1 on cell proliferation and the inhibitory effects on cell apoptosis.
Conclusion: MiR-34a inhibits cell proliferation and induces apoptosis in human NPC by targeting MCM3AP-AS1.

Keywords: MCM3AP-AS1, miR-34a, nasopharyngeal carcinoma, proliferation, apoptosis

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