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MicroRNA-206 inhibits the proliferation, migration and invasion of colorectal cancer cells by regulating the c-Met/AKT/GSK-3β pathway
被引:14
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.
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页数:8
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