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Knockdown of miR-194-5p inhibits cell proliferation, migration and invasion in breast cancer by regulating the Wnt/β-catenin signaling pathway

Breast cancer is a major public health concern, due to its increasing incidence and limited effective treatment. The present study aimed to investigate the expression of microRNA (miR)-194-5p and its roles in breast cancer. The expression levels of miR-194-5p and SRY-box 17 (SOX17) mRNA were detecte...

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Autores principales: Yang, Feibiao, Xiao, Zhangsheng, Zhang, Songze
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6202083/
https://www.ncbi.nlm.nih.gov/pubmed/30272253
http://dx.doi.org/10.3892/ijmm.2018.3897
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author Yang, Feibiao
Xiao, Zhangsheng
Zhang, Songze
author_facet Yang, Feibiao
Xiao, Zhangsheng
Zhang, Songze
author_sort Yang, Feibiao
collection PubMed
description Breast cancer is a major public health concern, due to its increasing incidence and limited effective treatment. The present study aimed to investigate the expression of microRNA (miR)-194-5p and its roles in breast cancer. The expression levels of miR-194-5p and SRY-box 17 (SOX17) mRNA were detected in breast cancer tissues and cell lines by reverse transcription-quantitative polymerase chain reaction. The protein expression levels were determined by western blotting. In addition, MTT, colony formation, scratch and Transwell assays were use to evaluate the characteristics of MCF-7 cells with miR-194-5p knockdown. The target verification of miR-194-5p was determined by luciferase reporter assay. Furthermore, tumor-bearing nude mice with miR-194-5p knockdown were used to assess the effects of miR-194-5p on tumor activity. In breast cancer tissues, miR-194-5p was upregulated, whereas SOX17 was downregulated. In addition, the expression levels of SOX17 and phosphorylated (p)-β-catenin in the cytosol and nucleus were increased in the miR-194-5p inhibitor group. In addition, cell proliferation, migration and invasion were inhibited in response to miR-194-5p knockdown. The luciferase reporter assay confirmed that SOX17 was a target gene of miR-194-5p. In the mouse studies, knockdown of miR-194-5p suppressed tumor growth and promoted SOX17 expression in nude mice with breast cancer. These findings suggested that knockdown of miR-194-5p may increase the expression of SOX17 and regulate the Wnt/β-catenin signaling pathway in breast cancer cells; therefore, miR-194-5p may be considered a potential target for breast cancer prevention.
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spelling pubmed-62020832018-11-07 Knockdown of miR-194-5p inhibits cell proliferation, migration and invasion in breast cancer by regulating the Wnt/β-catenin signaling pathway Yang, Feibiao Xiao, Zhangsheng Zhang, Songze Int J Mol Med Articles Breast cancer is a major public health concern, due to its increasing incidence and limited effective treatment. The present study aimed to investigate the expression of microRNA (miR)-194-5p and its roles in breast cancer. The expression levels of miR-194-5p and SRY-box 17 (SOX17) mRNA were detected in breast cancer tissues and cell lines by reverse transcription-quantitative polymerase chain reaction. The protein expression levels were determined by western blotting. In addition, MTT, colony formation, scratch and Transwell assays were use to evaluate the characteristics of MCF-7 cells with miR-194-5p knockdown. The target verification of miR-194-5p was determined by luciferase reporter assay. Furthermore, tumor-bearing nude mice with miR-194-5p knockdown were used to assess the effects of miR-194-5p on tumor activity. In breast cancer tissues, miR-194-5p was upregulated, whereas SOX17 was downregulated. In addition, the expression levels of SOX17 and phosphorylated (p)-β-catenin in the cytosol and nucleus were increased in the miR-194-5p inhibitor group. In addition, cell proliferation, migration and invasion were inhibited in response to miR-194-5p knockdown. The luciferase reporter assay confirmed that SOX17 was a target gene of miR-194-5p. In the mouse studies, knockdown of miR-194-5p suppressed tumor growth and promoted SOX17 expression in nude mice with breast cancer. These findings suggested that knockdown of miR-194-5p may increase the expression of SOX17 and regulate the Wnt/β-catenin signaling pathway in breast cancer cells; therefore, miR-194-5p may be considered a potential target for breast cancer prevention. D.A. Spandidos 2018-12 2018-09-25 /pmc/articles/PMC6202083/ /pubmed/30272253 http://dx.doi.org/10.3892/ijmm.2018.3897 Text en Copyright: © Yang et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Yang, Feibiao
Xiao, Zhangsheng
Zhang, Songze
Knockdown of miR-194-5p inhibits cell proliferation, migration and invasion in breast cancer by regulating the Wnt/β-catenin signaling pathway
title Knockdown of miR-194-5p inhibits cell proliferation, migration and invasion in breast cancer by regulating the Wnt/β-catenin signaling pathway
title_full Knockdown of miR-194-5p inhibits cell proliferation, migration and invasion in breast cancer by regulating the Wnt/β-catenin signaling pathway
title_fullStr Knockdown of miR-194-5p inhibits cell proliferation, migration and invasion in breast cancer by regulating the Wnt/β-catenin signaling pathway
title_full_unstemmed Knockdown of miR-194-5p inhibits cell proliferation, migration and invasion in breast cancer by regulating the Wnt/β-catenin signaling pathway
title_short Knockdown of miR-194-5p inhibits cell proliferation, migration and invasion in breast cancer by regulating the Wnt/β-catenin signaling pathway
title_sort knockdown of mir-194-5p inhibits cell proliferation, migration and invasion in breast cancer by regulating the wnt/β-catenin signaling pathway
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6202083/
https://www.ncbi.nlm.nih.gov/pubmed/30272253
http://dx.doi.org/10.3892/ijmm.2018.3897
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