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miR-325-3p Promotes the Proliferation, Invasion, and EMT of Breast Cancer Cells by Directly Targeting S100A2

This study was designed to investigate the precise mechanisms of miR-325-3p/S100A2 axis in breast cancer (BC). In this study, we found that the level of miR-325-3p was dramatically increased in BC tissues and cell lines, and the expression of S100A2 was significantly decreased. Also, the high level...

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Detalles Bibliográficos
Autores principales: Wang, Huiling, Hu, Xin, Yang, Feng, Xiao, Hui
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Cognizant Communication Corporation 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8420903/
https://www.ncbi.nlm.nih.gov/pubmed/33419488
http://dx.doi.org/10.3727/096504020X16100888208039
Descripción
Sumario:This study was designed to investigate the precise mechanisms of miR-325-3p/S100A2 axis in breast cancer (BC). In this study, we found that the level of miR-325-3p was dramatically increased in BC tissues and cell lines, and the expression of S100A2 was significantly decreased. Also, the high level of miR-325-3p was closely associated with low expression of S100A2 in BC tissues. Moreover, introduction of miR-325-3p significantly promoted proliferation, invasion, and EMT of BC cells. Bioinformatics analysis predicted that the S100A2 was a potential target gene of miR-325-3p. Luciferase reporter assay demonstrated that miR-325-3p could directly target S100A2. In addition, miR-325-3p overexpression had similar effects with knockdown of S100A2 on BC cells. Overexpression of S100A2 in BC cells partially reversed the promoted effects of miR-325-3p mimic. Overexpression of miR-325-3p promoted cell proliferation, invasion, and EMT of BC cells by directly downregulating S100A2 expression.