Breast cancer (BC) is one of the most common
malignancies occurring in women worldwide, and its incidence is increasing each year. Accumulating evidence indicated that
Myosin VI (MYO6) functions as a gene associated with
tumor progression in several
cancers. However, the potential role of MYO6 and its underlying mechanisms in the development and progression of BC remains unknown. Herein, we examined the expression levels of MYO6 in BC cells and tissues by western blot and immunohistochemistry. Loss- and gain-of-function investigations in vitro were performed to determine the
biological functions of MYO6. And in vivo effects of MYO6 on
tumorigenesis were investigated in nude mice. Our findings showed that the expression of MYO6 was up-regulated in
breast cancer, and its high expression was correlated with poor prognosis. Further investigation exhibited that silencing the expression of MYO6 significantly inhibited cell proliferation, migration and invasion, whereas overexpression of MYO6 enhanced these abilities in vitro. Also, reduced expression of MYO6 significantly retarded the
tumor growth in vivo. Mechanistically, Gene Set Enrichment Analysis (GSEA) revealed that MYO6 was involved in
mitogen-activated protein kinase (MAPK) pathway. Moreover, we proved that MYO6 enhanced BC proliferation, migration and invasion via increasing the expression of phosphorylated ERK1/2. Taken together, our findings highlight the role of MYO6 in promoting BC cell progression through MAPK/ERK pathway, suggesting it may be a new potential therapeutic and prognostic target for BC patients.