miR‑302d‑3p regulates the viability, migration and apoptosis of breast cancer cells through regulating the TMBIM6‑mediated ERK signaling pathway

MicroRNAs (miRs/miRNAs) play important roles in the occurrence, metastasis and prognosis of multiple types of cancers. However, the specific role of miR‑302d‑3p and its underlying mechanism in breast Cancer (BC) have not yet been reported. The present study aimed to identify the role of miR‑302D‑3p in BC and its potential mechanism using BC cell lines MCF7 and MDA‑MB‑231 and normal breast epithelial cell MCF‑10A. Cancer and paracancerous tissue from patients with BC were also used. Reverse transcription‑quantitative PCR was performed to detect the expression of miR‑302d‑3p and transmembrane Bax Inhibitor motif containing 6 (TMBIM6). Dual‑luciferase reporter assays verified the binding sites of miR‑302d‑3p and TMBIM6. Immunohistochemistry was used to measure the expression of TMBIM6. Cell Transfection techniques were used to overexpress or interfere with miR‑302d‑3p and TMBIM6. A Cell Counting Kit‑8 assay was performed to detect cell viability, and migration was measured using a wound healing assay. Apoptosis was detected by flow cytometry. The expression levels of apoptosis‑related proteins and pathway‑related proteins were detected by western blotting. The expression of miR‑302d‑3p in BC cell lines was found to be downregulated. It was also demonstrated that miR‑302d‑3p could inhibit cell viability and migration and promote Apoptosis. The expression of TMBIM6 in BC cell lines and tissues was upregulated. Upregulated miR‑302d‑3p was shown to inhibit viability and migration, and promote Apoptosis by targeting TMBIM6, during which extracellular signal‑regulated kinase (ERK) and its phosphorylation were inhibited in the ERK signaling pathway in cells. Overall, the present study demonstrated that miR‑302d‑3p could regulate the viability, migration and Apoptosis of BC cells through regulating TMBIM6‑mediated ERK signaling pathway.