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Role of microRNA-150-5p/SRCIN1 axis in the progression of breast cancer

In China, breast cancer is the most commonly occurring cancer in women. MicroRNAs (miRs) are a group of endogenous small non-coding RNAs, which serve a role in many biological processes through the regulation of target genes. In the current study, miR-150-5p expression was significantly up-regulated...

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Detalles Bibliográficos
Autores principales: Lu, Qingfu, Guo, Zhaoji, Qian, Haixin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6396020/
https://www.ncbi.nlm.nih.gov/pubmed/30867707
http://dx.doi.org/10.3892/etm.2019.7206
Descripción
Sumario:In China, breast cancer is the most commonly occurring cancer in women. MicroRNAs (miRs) are a group of endogenous small non-coding RNAs, which serve a role in many biological processes through the regulation of target genes. In the current study, miR-150-5p expression was significantly up-regulated in breast cancer tissues and cell lines. To investigate the cellular function and underlying molecular mechanism of miR-150-5p in breast cancer, TargetScan7.2 was used to identify miR-150-5p target genes. SRC kinase signaling inhibitor 1 (SRCIN1) was identified as a direct target gene of miR-150-5p and the current study demonstrated that SRCIN1 was negatively regulated by miR-150-5p in breast cancer cells. Furthermore, SRCIN1 expression was significantly down-regulated in breast cancer tissues and cell lines. Taken together, these results demonstrated that there was a negative association between miR-150-5p and SRCIN1 in breast cancer. The CCK-8 and Transwell assays were used to examine breast cancer cell viability, invasion and migration ability. The current study demonstrated that over-expression of miR-150-5p enhanced breast cancer cell proliferation, invasion and migration. In addition, miR-150-5p over-expression increased the expression of mesenchymal cell markers (vimentin, N-cadherin and β-catenin) and decreased the expression of epithelial cell markers (E-cadherin and zonula occludens-1). By contrast, miR-150-5p knockdown inhibited breast cancer cell viability, invasion and migration. Additionally, miR-150-5p knockdown decreased the expression of mesenchymal cell markers and increased the expression of epithelial cell markers. Taken together, these results suggest that the miR-150-5p/SRCIN1 axis may be a potential target in the treatment of breast cancer.