MiR-186 Inhibited Migration of NSCLC via Targeting cdc42 and Effecting EMT Process
Ying Dong1, Xintian Jin2, Zhiqiang Sun3, Yueming Zhao4, and Xianjing Song5,*
1Department of Radiotherapy, The Tumor Hospital of Jilin Province, Changchun 130021, China, 2Department of Thoracic, The Tumor Hospital of Jilin Province, Changchun 130021, China, 3Department of Invasive Technology, The Tumor Hospital of Jilin Province, Changchun 130021, China, 4Department of Oncology, The Tumor Hospital of Jilin Province, Changchun 130021, China, 5Department of Cardiology, The Second Hospital of Jilin University, Changchun 130041, China
*Correspondence: xianjingsong@yeah.net
Received November 29, 2016; Revised January 16, 2017; Accepted February 8, 2017.; Published online March 20, 2017.
© Korean Society for Molecular and Cellular Biology. All rights reserved.

This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License. To view a copy of this license, visit (http://creativecommons.org/licenses/by-nc-sa/3.0/).
ABSTRACT
In this study, qRT-PCR was employed to identify that miR-186 expression level in NSCLC tissues are highly associated with lymph node metastasis. In addition, through the application of western blotting, luciferase assay and qRT-PCR, it was found that miR-186 targeted 3'UTR of cdc42 mRNA and down-regulated cdc42 protein level in a post-transcriptional manner. Transwell assay indicated that cdc42 partially reversed the effect of miR-186 mimics. Besides, miR-186 was proved to regulate EMT by influencing biomarkers of this process and cell adhesion ability. Thus, miR-186 is a potential target for NSCLC therapy. miR-186 is proposed to be one of tumor-suppressors and may serve as a therapeutic target in NSCLC treatment.
Keywords: cdc42, EMT, migration, MiR-186, NSCLC


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