miR-214 inhibits epithelial-mesenchymal transition of breast cancer cells via downregulation of RNF8

被引:18
作者
Min, Lu [1 ]
Liu, Chuanyang [1 ]
Kuang, Jingyu [1 ]
Wu, Xiaomin [1 ]
Zhu, Lingyun [1 ]
机构
[1] Natl Univ Def Technol, Coll Liberal Arts & Sci, Dept Biol & Chem, Changsha 410073, Hunan, Peoples R China
基金
中国国家自然科学基金;
关键词
breast cancer; miR-214-RNF8; axis; EMT; HEPATOCELLULAR-CARCINOMA; OVARIAN-CANCER; MICRORNA-214; PROGRESSION; EXPRESSION; SURVIVAL; GROWTH; PROLIFERATION; SUPPRESSION; METASTASIS;
D O I
10.1093/abbs/gmz067
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
MicroRNAs (miRNAs) are a class of endogenous noncoding genes that regulate gene expression at the posttranscriptional level. In recent decades, miRNAs have been reported to play important roles in tumor growth and metastasis, while some reported functions of a specific miRNA in tumorigenesis are contradictory. In this study, we reevaluated the role of miR-214, which has been reported to serve as an oncogene or anti-oncogene in breast cancer metastasis. We found that miR-214 inhibited breast cancer via targeting RNF8, a newly identified regulator that could promote epithelial-mesenchymal transition (EMT). Specifically, the survival rate of breast cancer patients was positively correlated with miR-214 levels and negatively correlated with RNF8 expression. The overexpression of miR-214 inhibited cell proliferation and invasion of breast cancer, while suppression of miR-214 by chemically modified antagomir enhanced the proliferation and invasion of breast cancer cells. Furthermore, miR-214 could modulate the EMT process via downregulating RNF8. To our knowledge, this is the first report that reveals the role of the miR-214-RNF8 axis in EMT, and our results demonstrate a novel mechanism for miR-214 acting as a tumor suppressor through the regulation of EMT.
引用
收藏
页码:791 / 798
页数:8
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