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miR‐186 inhibits proliferation, migration, and epithelial‐mesenchymal transition in breast cancer cells by targeting Twist1
Author(s) -
Sun Wenjuan,
Zhang Yana,
Xue Peng
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.28283
Subject(s) - epithelial–mesenchymal transition , downregulation and upregulation , western blot , cancer research , malignancy , metastasis , twist transcription factor , breast cancer , microrna , mesenchymal stem cell , cancer , biology , medicine , pathology , gene , biochemistry
Objective Breast cancer (BC) is the most prevalent malignancy in women worldwide. Our study aimed to investigate the expression and biological effect of miR‐186 in BC. Methods Expression of miR‐186 was determined by quantitative reverse transcription PCR. Kaplan‐Meier curves were calculated for the survival data analysis. Functional assays were performed by 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide and wound healing assay. Protein expression was analyzed by Western blot. Results miR‐186 was downregulated in BC tissues and cells. Downregulation of miR‐186 was associated with tumor metastasis and a poor overall survival in patients with BC. Overexpression of miR‐186 inhibited BC cells proliferation, migration, and epithelial‐mesenchymal transition process; while suppression of miR‐186 exhibited an opposite effects on BC cells. In addition, Twist1 was identified as a direct target of miR‐186 in BC and restoration of Twist1 attenuated the biological effect of miR‐186 on BC cells. Conclusion Our findings suggest that miR‐186 functions as a tumor suppressor by targeting Twist1 in BC. miR‐186 may serve as a novel biomarker in BC diagnosis or a new therapeutic target in BC treatment.