[No authors listed]
Emerging evidence has demonstrated that microRNAs (miRNAs/miRs) have various biological functions in the development of human epidermal growth factor receptor 2 (HER2) positive breast cancer. The aim of the present study is to reveal the mechanism of miRâ193aâ3p inhibiting the progress of HER2 positive breast cancer. The expression of miRâ193aâ3p was evaluated by quantitative polymerase chain reaction (PCR). The methylation status of miRâ193aâ3p was evaluated by PCR and pyrosequencing analysis. Overexpression of miRâ193aâ3p and growth factor receptor bound protein 7 (GRB7) combined with in vitro tumorigenic assays were conducted to determine the carcinostatic capacities of miRâ193aâ3p in HER2 positive breast cancer cells. The association between miRâ193aâ3p and GRB7 was determined by luciferase reporter assay. Protein level was evaluated using western blot analysis. miRâ193aâ3p was downregulated in HER2 positive breast cancer cells and clinical tissues. Methylationâmediated silencing led to decreased expression of miRâ193aâ3p in HER2 positive breast cancer. Overexpression of miRâ193aâ3p could inhibit proliferation, migration and invasion of breast cancer cells. Overexpression of GRB7 could abolish this effect. miRâ193aâ3p could directly target the 3' untranslated region of GRB7. miRâ193aâ3p could directly or indirectly target extracellular signalâregulated kinase 1/2 (ERK1/2) and forkhead box M1 (FOXM1) signaling. In conclusion, it was identified that silencing of miRâ193aâ3p through hypermethylation can promote HER2 positive breast cancer progress by targeting GRB7, ERK1/2 and FOXM1 signaling. The function of miRâ193aâ3p in HER2 positive breast cancer implicates its potential application in therapy.
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