RETRACTED: MiR-361-5p inhibits the mobility of gastric cancer cells through suppressing epithelial-mesenchymal transition via the Wnt/β-catenin pathway (Retracted article. See vol. 809, 2022)

被引:24
作者
Tian, Lei [1 ]
Zhao, Zhifeng [2 ]
Xie, Ling [3 ]
Zhu, JinPeng [1 ]
机构
[1] Jinzhou Med Univ, Dept Gastroenterol, Affilliated Hosp 1, 2 Fifth Duan,People St, Jinzhou 121000, Liaoning, Peoples R China
[2] Zhongguo Med Univ, Dept Gastroenterol, Affilliated Hosp 4, Shenyang 110000, Liaoning, Peoples R China
[3] Jinzhou Med Univ, Dept Anat, Jinzhou 121000, Liaoning, Peoples R China
关键词
MiR-361-5p; Gastric cancer; EMT; Wnt/beta-catenin; GROWTH; METASTASIS; MICRORNAS; EMT;
D O I
10.1016/j.gene.2018.06.095
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
MiR-361-5p has been reported to be dysregulated in several types of cancers. However, the function of miR-3615p in gastric cancer (GC) is still not clear. In our present study, we aimed to investigate the effects of miR-361-5p in the mobility of GC and its potential mechanism. We found that miR-361-5p was significantly decreased in GC cell lines and tumor tissues. Decreased miR-361-5p expression was correlated with larger tumor size and advanced TNM stage. Functional analysis revealed that overexpression of miR-361-5p inhibited cell proliferation and mobility through suppressing the expression of MMP-3, MMP-9 and VEGF. Moreover, the expression of epithelial marker E-cadherin was increased while the expression of mesenchymal marker (Snail, N-cadherin, bcatenin) and Wnt/beta-catenin pathway related proteins (TCF4, Cyclin-D1, c-Myc) was increased by overexpression of miR-361-5p, indicating that overexpression of miR-361-5p suppressed epithelial-mesenchymal transition (EMT) via inhibiting Wnt/beta-catenin pathway in GC cells. In order to further verify our conjecture that miR-3615p mimic inhibited cell mobility through suppressing EMT via Wnt/beta-catenin pathway in GC, the Wnt/beta-catenin pathway activator LiC1 was used in this study. Our data showed that activation of Wnt/beta-catenin pathway by LiCI counteracted the regulating roles of miR-361-5p mimic through promoting EMT and cell mobility. In addition, TCF4 was knockdown and overexpressed in GC cells, and the results convinced the involvement of Wnt pathway in the regulation of EMT. Finally, results from in vivo experiments suggested that overexpression of miR-361-5p suppressed tumor growth and the expression of VEGF markedly through inhibiting EMT via the Wnt/beta-catenin pathway in GC nude mice. Taken together, our in vitro and in vivo experiments indicated that miR-361-5p suppressed cell mobility in GC through the inhibition of EMT via Wnt/beta-catenin pathway. Our findings indicated that miR-361-5p could be a promising therapeutic target for GC treatment.
引用
收藏
页码:102 / 109
页数:8
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