MicroRNAs target the Wnt/β-catenin signaling pathway to regulate epithelial-mesenchymal transition in cancer

被引：54
|
作者：
Lei, Yuhe [1 ]
Chen, Lei [1 ]
Zhang, Ge [2 ]
Shan, Aiyun [1 ]
Ye, Chunfeng [3 ]
Liang, Bin [4 ]
Sun, Jiayu [1 ]
Liao, Xin [1 ]
Zhu, Changfeng [1 ]
Chen, Yueyue [4 ]
Wang, Jing [4 ]
Zhang, Enxin [5 ]
Deng, Lijuan [4 ]
机构：
[1] Guangzhou Univ Chinese Med, Shenzhen Hosp, Dept Pharm, Shenzhen 518000, Guangdong, Peoples R China
[2] Guangdong Prov Hosp Chinese Med, Dept Big Data Res Chinese Med, Guangzhou 510120, Guangdong, Peoples R China
[3] Nanchang Univ, Affiliated Hosp 2, Dept Pediat, Nanchang 330006, Jiangxi, Peoples R China
[4] Jinan Univ, Formula Pattern Res Ctr, Sch Tradit Chinese Med, 605 Huangpu Ave West, Guangzhou 510632, Guangdong, Peoples R China
[5] Guangzhou Univ Chinese Med, Shenzhen Hosp, Dept Oncol, 6001 Beihuan Ave, Shenzhen 518000, Guangdong, Peoples R China
来源：
ONCOLOGY REPORTS | 2020年 / 44卷 / 04期
基金：
中国国家自然科学基金;
关键词：
microRNA; Wnt/beta-catenin signaling; epithelial-mesenchymal transition; cancer metastasis; cancer therapy; CELL LUNG-CANCER; BETA-CATENIN; E-CADHERIN; HEPATOCELLULAR-CARCINOMA; PANCREATIC-CANCER; COLORECTAL-CANCER; DOWN-REGULATION; INHIBITS PROLIFERATION; POSTTRANSCRIPTIONAL REGULATION; NUCLEAR TRANSLOCATION;
D O I：
10.3892/or.2020.7703
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
Epithelial-mesenchymal transition (EMT), during which cancer cells lose the epithelial phenotype and gain the mesenchymal phenotype, has been verified to result in tumor migration and invasion. Numerous studies have shown that dysregulation of the Wnt/beta-catenin signaling pathway gives rise to EMT, which is characterized by nuclear translocation of beta-catenin and E-cadherin suppression. Wnt/beta-catenin signaling was confirmed to be affected by microRNAs (miRNAs), several of which are down- or upregulated in metastatic cancer cells, indicating their complex roles in Wnt/beta-catenin signaling. In this review, we demonstrated the targets of various miRNAs in altering Wnt/beta-catenin signaling to promote or inhibit EMT, which may elucidate the underlying mechanism of EMT regulation by miRNAs and provide evidence for potential therapeutic targets in the treatment of invasive tumors.
引用
收藏
页码：1299 / 1313
页数：15
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