The crosstalk between microRNAs and the Wnt/β-catenin signaling pathway in cancer

被引:116
|
作者
Peng, Yin [1 ,4 ]
Zhang, Xiaojing [1 ,3 ]
Feng, Xianling [1 ]
Fan, Xinmim [1 ]
Jin, Zhe [1 ,2 ,3 ]
机构
[1] Shenzhen Univ, Sch Med, Dept Pathol, Shenzhen, Guangdong, Peoples R China
[2] Shenzhen Univ, Sch Med, Shenzhen Key Lab Micromol Innovatal Drugs, Shenzhen, Guangdong, Peoples R China
[3] Shenzhen Univ, Sch Med, Shenzhen Key Lab Translat Med Tumors, Shenzhen, Guangdong, Peoples R China
[4] Wuhan Univ, Sch Basic Med Sci, Dept Pathol, Wuhan, Hubei, Peoples R China
基金
中国博士后科学基金;
关键词
microRNA; Wnt/beta-catenin signaling pathway; cancer; EPITHELIAL-MESENCHYMAL-TRANSITION; HUMAN GASTRIC-CANCER; CELL LUNG-CANCER; NASOPHARYNGEAL CARCINOMA RADIORESISTANCE; HUMAN HEPATOCELLULAR-CARCINOMA; ADENOMATOUS POLYPOSIS-COLI; HUMAN BLADDER-CANCER; NEMO-LIKE KINASE; BETA-CATENIN; COLORECTAL-CANCER;
D O I
10.18632/oncotarget.12923
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Mounting evidence has indicated microRNA (miR) dysregulation and the Wnt/ beta-catenin signaling pathway jointly drive carcinogenesis, cancer metastasis, and drug-resistance. The current review will focus on the role of the crosstalk between miRs and the Wnt/beta-catenin signaling pathway in cancer development. MiRs were found to activate or inhibit the canonical Wnt pathway at various steps. On the other hand, Wnt activation increases expression of miR by directly binding to its promoter and activating transcription. Moreover, there are mutual feedback loops between some miRs and the Wnt/beta-catenin signaling pathway. Clinical trials of miR-based therapeutic agents are investigated for solid and hematological tumors, however, challenges concerning low bio availability and possible side effects must be overcome before the final clinical application. This review will describe current understanding of miR crosstalk with the Wnt/beta-catenin signaling cascade. Better understanding of the regulatory network will provide insight into miR-based therapeutic development.
引用
收藏
页码:14089 / 14106
页数:18
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