MicroRNA‑125a‑5p controls the proliferation, apoptosis, migration and PTEN/MEK1/2/ERK1/2 signaling pathway in MCF‑7 breast cancer cells

Abstract

MicroRNA (miR)-125a-5p has shown the potential for suppressing tumorigenesis and development; however, the effects of miR-125a-5p on breast cancer cells remains unknown. The aim of this study was to evaluate the effects and underlying mechanisms of miR-125a-5p in MCF-7 breast cancer cells. MCF-7 cells were transfected with miR-125a-5p mimic or miR-125a-5p small interfering RNA to produce miR-125a-5p overexpressing/knockdown cells. Cell proliferation was assessed by an MTT assay, and cell migration ability was determined by an in vitro scratch assay. Hoechst 33258 staining and flow cytometry were performed to assess the effects of miR-125a-5p on MCF-7 apoptosis. Western blotting and reverse transcription-quantitative polymerase chain reaction were used for measuring phosphatase and tensin homolog (PTEN), phosphorylated (p)-mitogen-activated protein kinase kinase (MEK1/2)/MEK1/2, p-ERK1/2/ERK1/2, B-cell lymphoma-2 (Bcl-2), cleaved caspase-3, and miR-125a-5p expression. miR-125a-5p overexpression inhibited the proliferation and migration, but promoted the apoptosis of MCF-7 cells. These effects were associated with increases in PTEN and cleaved caspase-3 expression, and decreases in p-MEK1/2/MEK1/2, p-ERK1/2/ERK1/2, and Bcl-2. Silencing of miR-125a-5p exhibited opposing effects on MCF-7 cells. These observations suggested that miR-125a-5p participates in the regulation of multiple functions of MCF-7 cells by promoting the expression of PTEN tumor suppressor genes, activating MEK1/2/ERK1/2 signaling, and regulating caspase-3/Bcl-2 signaling. Thus, it may be a suitable target for breast cancer gene therapy.