MiR-133 Targets YES1 and Inhibits the Growth of Triple-Negative Breast Cancer Cells

• Published in: Technology in cancer research & treatment Vol. 19; p. 1533033820927011
• Main Authors: Zhang, Guochen, Wang, Junlan, Zheng, Ruilin, Song, Beibei, Huang, Li, Liu, Yujiang, Hao, Yating, Bai, Xiangdong
• Format: Journal Article
• Language: English
• Published: Los Angeles, CA SAGE Publications 2020; Sage Publications Ltd; SAGE Publishing
• Subjects: 3' Untranslated regions; Adaptor Proteins, Signal Transducing - genetics; Adaptor Proteins, Signal Transducing - metabolism; Apoptosis; Biomarkers, Tumor - genetics; Biomarkers, Tumor - metabolism; Breast cancer; Cell Movement; Cell Proliferation; Colonies; Female; Gene Expression Regulation, Neoplastic; Humans; MicroRNAs - genetics; Middle Aged; miRNA; Original; Phosphorylation; Prognosis; Proto-Oncogene Proteins c-yes - genetics; Proto-Oncogene Proteins c-yes - metabolism; Transcription Factors - genetics; Transcription Factors - metabolism; Triple Negative Breast Neoplasms - genetics; Triple Negative Breast Neoplasms - pathology; Triple Negative Breast Neoplasms - surgery; Tumor cell lines; Tumor Cells, Cultured; Yes-associated protein; YAP1; YES1; TNBC; miR-133
• ISSN: 1533-0346; 1533-0338
• DOI: 10.1177/1533033820927011

Triple-negative breast cancer shows worse outcome compared with other subtypes of breast cancer. The discovery of dysregulated microRNAs and their roles in the progression of triple-negative breast cancer provide novel strategies for the treatment of patients with triple-negative breast cancer. In this study, we identified the significant reduction of miR-133 in triple-negative breast cancer tissues and cell lines. Ectopic overexpression of miR-133 suppressed the proliferation, colony formation, and upregulated the apoptosis of triple-negative breast cancer cells. Mechanism study revealed that the YES Proto-Oncogene 1 was a target of miR-133. miR-133 bound the 3′-untranslated region of YES Proto-Oncogene 1 and decreased the level of YES Proto-Oncogene 1 in triple-negative breast cancer cells. Consistent with miR-133 downregulation, YES1 was significantly increased in triple-negative breast cancer, which was inversely correlated with the level of miR-133. Restoration of YES Proto-Oncogene 1 attenuated the inhibitory effects of miR-133 on the proliferation and colony formation of triple-negative breast cancer cells. Consistent with the decreased expression of YES Proto-Oncogene 1, overexpression of miR-133 suppressed the phosphorylation of YAP1 in triple-negative breast cancer cells. Our results provided novel evidence for the role of miR-133/YES1 axis in the development of triple-negative breast cancer, which indicated miR-133 might be a potential therapeutic strategy for triple-negative breast cancer.