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MiR-133 Targets YES1 and Inhibits the Growth of Triple-Negative Breast Cancer Cells
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 t...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
SAGE Publications
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7278099/ https://www.ncbi.nlm.nih.gov/pubmed/32462982 http://dx.doi.org/10.1177/1533033820927011 |
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author | Zhang, Guochen Wang, Junlan Zheng, Ruilin Song, Beibei Huang, Li Liu, Yujiang Hao, Yating Bai, Xiangdong |
author_facet | Zhang, Guochen Wang, Junlan Zheng, Ruilin Song, Beibei Huang, Li Liu, Yujiang Hao, Yating Bai, Xiangdong |
author_sort | Zhang, Guochen |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-7278099 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | SAGE Publications |
record_format | MEDLINE/PubMed |
spelling | pubmed-72780992020-06-17 MiR-133 Targets YES1 and Inhibits the Growth of Triple-Negative Breast Cancer Cells Zhang, Guochen Wang, Junlan Zheng, Ruilin Song, Beibei Huang, Li Liu, Yujiang Hao, Yating Bai, Xiangdong Technol Cancer Res Treat Original Article 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. SAGE Publications 2020-05-28 /pmc/articles/PMC7278099/ /pubmed/32462982 http://dx.doi.org/10.1177/1533033820927011 Text en © The Author(s) 2020 https://creativecommons.org/licenses/by-nc/4.0/ This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage). |
spellingShingle | Original Article Zhang, Guochen Wang, Junlan Zheng, Ruilin Song, Beibei Huang, Li Liu, Yujiang Hao, Yating Bai, Xiangdong MiR-133 Targets YES1 and Inhibits the Growth of Triple-Negative Breast Cancer Cells |
title | MiR-133 Targets YES1 and Inhibits the Growth of Triple-Negative
Breast Cancer Cells |
title_full | MiR-133 Targets YES1 and Inhibits the Growth of Triple-Negative
Breast Cancer Cells |
title_fullStr | MiR-133 Targets YES1 and Inhibits the Growth of Triple-Negative
Breast Cancer Cells |
title_full_unstemmed | MiR-133 Targets YES1 and Inhibits the Growth of Triple-Negative
Breast Cancer Cells |
title_short | MiR-133 Targets YES1 and Inhibits the Growth of Triple-Negative
Breast Cancer Cells |
title_sort | mir-133 targets yes1 and inhibits the growth of triple-negative
breast cancer cells |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7278099/ https://www.ncbi.nlm.nih.gov/pubmed/32462982 http://dx.doi.org/10.1177/1533033820927011 |
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