MiR-186 Inhibited Migration of NSCLC via Targeting cdc42 and Effecting EMT Process

被引：34
|
作者：
Dong, Ying [1 ]
Jin, Xintian [2 ]
Sun, Zhiqiang [3 ]
Zhao, Yueming [4 ]
Song, Xianjing [5 ]
机构：
[1] Tumor Hosp Jilin Prov, Dept Radiotherapy, Changchun 130021, Peoples R China
[2] Tumor Hosp Jilin Prov, Dept Thorac, Changchun 130021, Peoples R China
[3] Tumor Hosp Jilin Prov, Dept Invas Technol, Changchun 130021, Peoples R China
[4] Tumor Hosp Jilin Prov, Dept Oncol, Changchun 130021, Peoples R China
[5] Jilin Univ, Hosp 2, Dept Cardiol, Changchun 130041, Peoples R China
来源：
MOLECULES AND CELLS | 2017年 / 40卷 / 03期
关键词：
cdc42; EMT; migration; MiR-186; NSCLC; CELL-PROLIFERATION; 3RD-LINE TREATMENT; CANCER; EXPRESSION; MICRORNAS; INVASION; MIR-B-10;
D O I：
10.14348/molcells.2017.2291
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
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.
引用
收藏
页码：195 / 201
页数：7
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