MicroRNA-182 suppresses clear cell renal cell carcinoma migration and invasion by targeting IGF1R

被引:25
|
作者
Wang, X. [1 ,2 ]
Li, H. [2 ]
Cui, L. [2 ]
Feng, J. [3 ]
Fan, Q. [1 ]
机构
[1] Zhengzhou Univ, Affiliated Hosp 1, Dept Oncol, Zhengzhou 450052, Henan, Peoples R China
[2] Zhengzhou Univ, Affiliated Hosp 1, Dept Pathol, Zhengzhou 450052, Henan, Peoples R China
[3] Zhengzhou YIHE Hosp, Dept Resp Med, Zhengzhou 450047, Henan, Peoples R China
关键词
MicroRNA-182; clear cell renal cell carcinoma; migration and invasion; insulin-like growth factor 1 receptor; FACTOR-I RECEPTOR; GASTRIC-CANCER; METASTASIS; GROWTH; EXPRESSION; PROLIFERATION; CONTRIBUTES; MARKERS; MIR-182;
D O I
10.4149/neo_2016_508
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The purpose of our study was aimed to determine the functional role of microRNA (miR)-182 in clear cell renal cell carcinoma (ccRCC) and try to clarify its underlying molecular mechanism. Expression of miR-182 in both cancer and peripheral blood samples was analyzed by quantitative real-time PCR (qRT-PCR). Human RCC line Caki-1 cells were transfected with miR-182 mimic, miR-182 inhibitor, or negative controls, and then the cell viability, colony-formation ability, migration, and invasion assay were determined. Luciferase reporter assay, qRT-PCR and Western blotting were used to determine whether insulin-like growth factor 1 receptor (IGF1R) was a target of miR-182. Further, small interfering RNA (siRNA) against IGF1R was co-transfected with miR-182 inhibitor into cells, and then the effects on migration and invasion were assessed. MiR-182 was down-regulated in both cancer and blood samples compared to the matched non-tumor adjacent tissues and healthy volunteers, respectively (both P<0.05). Compared to the control group, cell viability, colony-forming ability, and numbers of migrated and invaded cells were significantly decreased by transfection with miR-182 mimic but were markedly increased by miR-182 inhibitor (all P < 0.05). Luciferase reporter assay confirmed that IGF1R was a target gene of miR-182, and IGF1R was negatively regulated by miR-182. Co-transfection of miR-182 inhibitor with si-IGF1R reversed the effect of miR-182 inhibitor on the migration and invasion of the cells. MiR-182 functions as an anti-oncogene in ccRCC, and miR-182-mediated inhibition of cell migration and invasion might be through directly targeting IGF1R.
引用
收藏
页码:717 / 725
页数:9
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