Affiliation:
1. Department of Surgery, Hunan Provincial Peoples Hospital (The First Affiliated Hospital of Hunan Normal University)ChangshaP.R. China
2. Department of Surgery, Hunan Childrens HospitalChangshaP.R. China
3. Department of Pharmacy, Hunan Provincial Peoples Hospital (The First Affiliated Hospital of Hunan Normal University)ChangshaP.R. China
Abstract
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.
Subject
Cancer Research,Oncology,General Medicine
Cited by
21 articles.
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