Back to Journals » Cancer Management and Research » Volume 12

LncRNA MIR503HG Inhibits Non-Small Cell Lung Cancer Cell Proliferation by Inducing Cell Cycle Arrest Through the Downregulation of Cyclin D1

Authors Xu S, Zhai S, Du T, Li Z

Received 15 August 2019

Accepted for publication 31 January 2020

Published 5 March 2020 Volume 2020:12 Pages 1641—1647

DOI https://doi.org/10.2147/CMAR.S227348

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Dr Ahmet Emre Eskazan


Shufen Xu,* Shengping Zhai,* Tiantian Du,* Zhan Li

Respiratory Department, Yantai Yuhuangding Hospital Affiliated to Qingdao University, Yantai City, Shandong Province 264000, People’s Republic of China

*These authors contributed equally to this work

Correspondence: Zhan Li
Respiratory Department, Yantai Yuhuangding Hospital Affiliated to Qingdao University, NO. 20 Yuhuangding East Road, Zhifu District, Yantai City, Shandong Province 264000, People’s Republic of China
Email gvjycert0951@126.com

Introduction: LncRNA MIR503HG has been reported to participate in liver cancer and ALK-negative anaplastic large-cell lymphoma, while its role in non-small cell lung cancer (NSCLC) is unknown. We therefore investigated the functions of lncRNA MIR503HG in NSCLC.
Methods: MIR503HG expression in paired cancer and non-cancer tissues from NSCLC patients was analyzed by RT-qPCR. The interaction between cyclin D1 and MIR503HG was analyzed by overexpression experiments. Cell cycle analysis was performed by flow cytometry. Cell proliferation was analyzed by CCK-8 assay.
Results: MIR503HG was downregulated in NSCLC and low levels of MIR503HG were associated with poor survival. In contrast, cyclin D1 was upregulated in NSCLC, and cyclin D1 and MIR503HG were inversely correlated. In NSCLC cells, overexpression experiments revealed that MIR503HG functioned as an upstream inhibitor of cyclin D1. MIR503HG overexpression led to G1 cell cycle arrest, while overexpression of cyclin D1 attenuated the effects of MIR503HG overexpression. Similarly, MIR503HG overexpression resulted in reduced cell proliferation rate, while overexpression of cyclin D1 caused the increased cell proliferation rate and attenuated effects of MIR503HG overexpression.
Conclusion: MIR503HG inhibits NSCLC cell proliferation by inducing cell cycle arrest through the downregulation of cyclin D1.

Keywords: non-small cell lung cancer, lncRNA MIR503HG, cyclin D1, cell cycle, survival

Creative Commons License This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License. By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.

Download Article [PDF]  View Full Text [HTML][Machine readable]