MicroRNA-206 inhibits the proliferation, migration and invasion of colorectal cancer cells by regulating the c-Met/AKT/GSK-3β pathway

被引:12
|
作者
Lyu, Jiayu [1 ]
Sun, Yao [2 ]
Li, Xizhi [3 ]
Ma, Huili [4 ]
机构
[1] Fifth Hosp Harbin, Dept Gen Surg 1, Harbin 150040, Heilongjiang, Peoples R China
[2] Heilongjiang Prov Land Reclamat Bur, Gen Hosp, Dept Neurol, Harbin 150088, Heilongjiang, Peoples R China
[3] Binzhou Med Univ Hosp, Dept Neurol, 661 Huanghe 2nd Rd, Binzhou 256603, Shandong, Peoples R China
[4] Binzhou Med Univ Hosp, Trauma Ctr, Dept Emergency Surg, 661 Huanghe 2nd Rd, Binzhou 256603, Shandong, Peoples R China
关键词
microRNA-206; c-Met; colorectal cancer; proliferation; migration; invasion; EPITHELIAL-MESENCHYMAL TRANSITION; C-MET; BREAST-CANCER; TARGETING MET; MIR-206; METASTASIS; GROWTH; ANGIOGENESIS; REPRESSES; GENE;
D O I
10.3892/ol.2020.12408
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
An imbalance in microRNA (miRNA/miR) expression is closely associated with tumorigenesis and progression. miR-206 is downregulated in different types of tumors, including colorectal cancer (CRC). However, the effects of miR-206 on the progression of CRC, and its underlying molecular mechanisms are yet to be elucidated. The present study aimed to investigate the effects of miR-206 on the proliferation, migration and invasion of colorectal cancer cells, and determine its potential molecular mechanism. The results of the present study demonstrated that the expression levels of miR-206 and c-Met were affected in HCT116 and SW480 cells by transfected with miR-206 mimic, inhibitor or small interfering RNA-c-Met. A Dual-luciferase reporter assay was performed to identify the miRNA targets. Cell proliferation, migration and invasion assays were also performed. The results demonstrated that overexpression of miR-206 significantly decreased the viability of HCT116 and SW480 cells. The results of the Transwell assay indicated that the cell migratory and invasive abilities were inhibited following transfection with miR-206 mimic. As a target of miR-206, knockdown of c-Met significantly suppressed cell viability, migration and invasion. In addition, c-Met knockdown or overexpression of miR-206 inhibited activation of the AKT/GSK-3 beta pathway. Collectively, these results suggest that miR-206 suppresses the proliferation, migration and invasion of CRC cells by targeting the c-Met/AKT/GSK-3 beta pathway.
引用
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页数:8
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