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miR-135 regulated breast cancer proliferation and epithelial-mesenchymal transition acts by the Wnt/β-catenin signaling pathway

Breast cancer (BC) is the most common cancer in women around the world. microRNAs (miRNAs/miRs) have been proved to be associated with the development and progression of breast cancer. In the present study, to elucidate the effects of dysregulated miR-135 on cells and underlying mechanisms in BC, in...

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Detalles Bibliográficos
Autores principales: Jiang, Daqiong, Zhou, Bo, Xiong, Yan, Cai, Hongbing
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6414157/
https://www.ncbi.nlm.nih.gov/pubmed/30720046
http://dx.doi.org/10.3892/ijmm.2019.4081
Descripción
Sumario:Breast cancer (BC) is the most common cancer in women around the world. microRNAs (miRNAs/miRs) have been proved to be associated with the development and progression of breast cancer. In the present study, to elucidate the effects of dysregulated miR-135 on cells and underlying mechanisms in BC, in vitro and in vivo experiments were conducted. The biological functions of miR-135 were studied using MTT, colony formation, wound healing, transwell assays as well as tumorigenicity analysis. Gain- and loss- of function of miR-135 studies revealed that ectopic expression of miR-135 in MDA-MB-468 and MCF-7 cells significantly inhibited cell growth, migration, invasion and EMT, at least in part through inhibiting the activation of the Wnt/β-catenin pathway. Moreover, this was reversed in cells which were transfected with miR-135 inhibitors. Taken together, the results of the present study provided evidence that miR-135 acted as a tumor suppressor in BC, which may represent a novel therapeutic strategy for the diagnosis and prognosis of BC.