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MicroRNA-671-3p promotes the proliferation and migration of glioma cells via targeting CKAP4

Authors Lu GF, You CY, Chen YS, Jiang H, Zheng X, Tang W, Wang X, Xu H, Geng F

Received 15 June 2018

Accepted for publication 22 August 2018

Published 25 September 2018 Volume 2018:11 Pages 6217—6226

DOI https://doi.org/10.2147/OTT.S177325

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Andrew Yee

Peer reviewer comments 3

Editor who approved publication: Dr Sanjeev Srivastava


Gui-Feng Lu,1 Chun-Yue You,2 Yuan-Shou Chen,3 Hui Jiang,3 Xiang Zheng,4 Wei-Wei Tang,1 Xian-Yan Wang,1 Hai-Yan Xu,1 Fei Geng3

1Department of Pathophysiology, Zunyi Medical University, Zunyi 563003, China; 2Department of Neurosurgery, The Affiliated Hospital of Zunyi Medical University, Zunyi 563003, China; 3Department of Physiology, Zunyi Medical University, Zunyi 563003, China; 4Department of Genetics, Zunyi Medical University, Zunyi 563003, China

Background and objective: Glioma is one of the most aggressive and malignant cancers originating from the human brain. Increasing evidence suggests that aberrant expression of microRNAs (miRNAs) frequently occurs in glioma and miRNAs are critical regulators of glioma. miR-671 has recently been revealed to be a novel miRNA that plays a vital role in human glioblastoma multiforme. However, the functional role and underlying mechanisms of miR-671-3p require further analysis.
Materials and methods: Western blot and fluorescence quantitative PCR were used to assess the expression of cytoskeleton-associated protein 4 (CKAP4) and miR-671-3p, respectively. A Cell Counting Kit-8 (CCK-8) assay and a Boyden chamber assay were used to detect the proliferative and migratory abilities of glioma cells. A luciferase assay was used to determine the target gene of miR-671-3p. Apoptosis was analyzed by flow cytometry.
Results: Our results revealed that overexpression of miR-671-3p promoted cell proliferation and migration in vitro. Meanwhile, forced expression of miR-671-3p reduced apoptosis. In contrast, inhibition of miR-671-3p had the opposite effects. We also identified CKAP4 to be a direct target of miR-671-3p. The expression levels of CKAP4 were decreased in clinical samples and inversely correlated with miR-671-3p expression levels. Ectopic expression of CKAP4 reversed the promotive activity of miR-671-3p in the proliferation and migration and enhanced apoptosis.
Conclusion: Our study demonstrates that miR-671-3p is a predominant positive regulator of glioma progression, thus providing new insights into the molecular mechanisms of glioma development. The findings suggest that the miR-6713p/CKAP4 axis may serve as a potential therapeutic target or biomarker in glioma.

Keywords: miR-671-3p, glioma, migration, proliferation, CKAP4

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