Abstract
Previous studies demonstrated that puerarin represents a potential therapeutic drug for breast cancer treatment, due to its ability to inhibit the migration of MCF‑7 and MDA‑MB‑231 cell lines. In order to investigate the mechanism of puerarin in breast cancer cells, the aim of the present study was to examine whether puerarin regulated the dual specificity phosphatase 1 (DUSP1) expression level by promoting the microRNA‑133a‑3p (miR‑133a‑3p) expression level in breast cancer. Cell viability and apoptosis were assessed in HCC38 cells by Cell Counting Kit‑8 assays and a flow cytometry assay, respectively. In total, four treatment groups were considered: Puerarin treatment, miR‑133a‑3p mimics transfection, puerarin + miR‑133a‑3p mimics and negative control. miR‑133a‑3p expression and DUSP1 mRNA expression levels were analyzed by reverse transcription‑quantitative polymerase chain reaction, and western blotting was used to detect the protein expression level. Furthermore, a luciferase reporter gene assay was used to test whether DUSP1 mRNA was a direct target of miR‑133a‑3p. The present results suggested that treatment with puerarin or miR‑133a‑3p mimics transfection affected the miR‑133a‑3p expression level and the activity of the DUSP1/p38 pathway, leading to inhibition of HCC38 cell viability and an increase in apoptosis. miR‑133a‑3p overexpression enhanced the drug action of peurarin. In conclusion, puerarin may increase DUSP1 expression by promoting the miR‑133a‑3p expression level in HCC38 breast cancer cells. Therefore, miR‑133a‑3p may represent a novel molecular marker for diagnosis and treatment of breast cancer, and puerarin may represent a promising clinical drug for treatment of patients with breast cancer.