The lncRNA BCYRN1 Functions as an Oncogene in Human Glioma by Downregulating miR-125a-5p in vitro
Authors Yu W, Xiang D, Jia H, He X, Sheng J, Long Y, Zhu S, Wang K, Liu Q
Received 15 August 2019
Accepted for publication 10 January 2020
Published 13 February 2020 Volume 2020:12 Pages 1151—1161
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Antonella D'Anneo
Wei Yu,1,* Dulei Xiang,1,* Houjun Jia,2,* Xin He,1 Jie Sheng,1 Yuxiang Long,1 Shujuan Zhu,1 Kejian Wang,1 Qian Liu1
1Institute of Neuroscience, Chongqing Medical University, Chongqing 400016, People’s Republic of China; 2Department of Gastrointestinal Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Qian Liu Tel +86 186 2355 1357
Introduction: Numerous studies have demonstrated that long noncoding RNAs (lncRNAs) are deregulated in many cancers and exert their functions through multiple cancer-related biological processes. Glioma is the most common primary malignant central nervous system tumor and has a high fatality rate in adults. In current study, we aimed to determine the role and functional mechanism of the lncRNA BCYRN1 in glioma.
Methods: Gain-of-function and loss-of function approaches were used to investigate the function of BCYRN1. The effects of BCYRN1 on glioma cell proliferation, migration and invasion were evaluated using MTS, Transwell and wound-healing assays. The correlation between the expression of BCYRN1 and miR-125a-5p was verified by quantitative real-time PCR.
Results: The upregulation of BCYRN1 promoted the proliferation, migration and invasion of glioma cells. Meanwhile, the knockdown of BCYRN1 had the opposite effects. BCYRN1 was negatively correlated with miR-125a-5p. Additionally, TAZ, the endogenous target of miR-125a-5p, could be regulated by BCYRN1 in RNA and protein levels. A miR-125a-5p inhibitor restored BCYRN1 siRNA function in glioma.
Conclusion: The present study indicates that BCYRN1 promotes glioma cell proliferation, invasion and migration in vitro. Mechanistically, upregulated expression of BCYRN1 in glioma acts as a sponge to sequester the endogenous tumor suppressor miR-125a-5p and to further increase the expression TAZ. Our findings suggest that BCYRN1 is a novel oncogene and a new therapeutic target for glioma.
Keywords: BCYRN1, glioma, miR-125a-5p, ceRNA, TAZ
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