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

癌基因 上皮-间质转换 小RNA 癌变 癌症研究 乳腺癌 转移 下调和上调 拮抗剂 癌症 生物 细胞生长 细胞周期 基因 遗传学
作者
Min Lu,Chuanyang Liu,Jingyu Kuang,Xiaomin Wu,Lingyun Zhu
出处
期刊:Acta Biochimica et Biophysica Sinica [Oxford University Press]
卷期号:51 (8): 791-798 被引量:18
标识
DOI:10.1093/abbs/gmz067
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.

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