已发表论文

lncRNA LINC01494 通过 miR-122-5p/CCNG1 轴促进神经胶质瘤的增殖、迁移和侵袭

 

Authors Li C, Hu G, Wei B, Wang L, Liu N

Received 24 April 2019

Accepted for publication 26 August 2019

Published 18 September 2019 Volume 2019:12 Pages 7655—7662

DOI https://doi.org/10.2147/OTT.S213345

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Ms Rachel Predeepa

Peer reviewer comments 3

Editor who approved publication: Dr Leo Jen-Liang Su

Background: Long noncoding RNAs (lncRNAs) are recognized as key effectors in tumor, including glioma. LINC01494 is an uncharacterized novel lncRNA. In this research, we aimed to investigate the function of LINC01494 in glioma.
Methods: Gene relative expression was analyzed by qRT-PCR method. CCK8, colony formation and Transwell assay was used to determine cell proliferation, migration and invasion. Bioinformatics analyses were used to predict the target of LINC01494 and miR-122-5p. Luciferase reporter assay was utilized to validate the interactions between LINC01494 and miR-122-5p or CCNG1 and miR-122-5p.
Results: LINC01494 was identified as a significantly upregulated lncRNA in glioma through bioinformatics analysis. Furthermore, LINC01494 upregulation indicated poor prognosis. Meanwhile, in vitro investigation indicated that silencing LINC01494 with siRNAs obviously inhibited the proliferation, cell cycle, migration and invasion of glioma cells. Besides, it is found that LINC01494 expression was negatively correlated with miR-122-5p. We demonstrated that LINC01494 inhibited miR-122-5p to upregulate CCNG1 expression through direct interaction. Rescue assay further demonstrated that LINC01494/miR-122-5p/CCNG1 signaling cascade plays a critical role in regulating glioma cell proliferation, migration and invasion.
Conclusion: Taken together, our findings demonstrated the essential function and molecular mechanism of LINC01494 in glioma progression.
Keywords: LINC01494, miR-122-5p, CCNG1, glioma, proliferation




Figure 3 LINC01494 overexpression promotes glioma progression...