Back to Journals » OncoTargets and Therapy » Volume 11

MicroRNA-486-3p directly targets BIK and regulates apoptosis and invasion in colorectal cancer cells

Authors Feng L, Jing L, Han J, Wang G, Liu Y, Zhang X, Wang Y, Wang F, Ma H, Liu Y

Received 16 July 2018

Accepted for publication 29 September 2018

Published 6 December 2018 Volume 2018:11 Pages 8791—8801

DOI https://doi.org/10.2147/OTT.S180354

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Andrew Yee

Peer reviewer comments 2

Editor who approved publication: Dr Yao Dai


Li Feng,1 Li Jing,1 Jing Han,1 Guiying Wang,2 Yan Liu,1 Xue Zhang,1 Yudong Wang,1 Feifei Wang,2 Hongqing Ma,2 Yibing Liu1

1Department of Medical Oncology, Fourth Hospital of Hebei Medical University, Shijiazhuang 050011, China; 2Second Department of General Surgery, Fourth Hospital of Hebei Medical University, Shijiazhuang 050011, China

Background: MicroRNAs influence almost every genetic pathway and are involved in colorectal cancer (CRC). However, the biological role of miR486-3p in CRC remains to be elucidated.
Methods:
In this study, miR486-3p expression in CRC cell lines and normal colonic epithelial cells was determined. After miR486-3p mimic, inhibitor, and BIK siRNA transfection, cell proliferation, apoptosis, and migration were examined. Furthermore, the target of miR486-3p was identified by luciferase-reporter assay and underlying molecular mechanisms studied.
Results: The results revealed that miR486-3p was significantly upregulated in CRC compared with normal colonic epithelial cells, whereas BIK expression was remarkably downregulated in CRC cells. MTT assays demonstrated that suppression of miR486-3p expression reduced CRC cell proliferation, whereas elevated miR486-3p or BIK silencing induced cell proliferation. Wound-healing assays and transwell experiments revealed that both upregulation of miR486-3p and downregulation of BIK increased CRC cell migration and invasion ability. Moreover, bioinformatic target prediction identified BIK as a putative target of miR486-3p. Knockdown of miR486-3p was shown to upregulate BIK expression, whereas overexpression of miR486-3p suppressed the expression of BIK. Luciferase reporter assay results further confirmed this deduction.
Conclusion: In conclusion, these findings suggest that miR486-3p is an oncogene in CRC. Gene therapy using miR486-3p inhibition may provide a new clue for CRC therapy.

Keywords: colorectal cancer, miR486-3p, BIK, apoptosis, invasion

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]