MicroRNA-142-3p chemo-sensitizing breast cancer to docetaxel: apoptosis and cell cycle arrest induction, and migration suppression.

Abstract

Docetaxel (DTX) is widely utilized in breast cancer treatment. However, cancer cell resistance has limited its anti-tumor efficacy. Some molecules called microRNAs (miRNAs), acting like fine-tuned switches, can influence how breast cancer develops and spreads. We conducted a study to examine if augmenting breast cancer cells with a particular molecule, known as miRNA-142-3p, could improve the efficacy of a widely used treatment called DTX. The expression level of miR-142-3p was initially assessed in MDA-MB-468 cells. The miRNA transfection was performed to conduct additional experiments. The impact of a combined treatment involving DTX and miRNA-142-3p on both cell migration (by wound healing assay) and apoptosis (using annexin V/Propidium iodide staining) was examined. Cell viability was determined through the MTT assay, and gene expression was quantified using quantitative real-time polymerase chain reaction. The combined application of DTX and miRNA-142-3p resulted in a significant decrease in the expression of factors promoting tumor growth, such as SOX2, Octamer 4, HMGA2, Kruppel-like factor 4, and Bach-1. Additionally, the combination of miRNA-142-3p and DTX initiated apoptotic cell death. Moreover, the progression of breast cancer cells was impeded by inducing cell cycle arrest at the G¹ phase. This combination also efficiently restrained the migration and invasion of breast cancer cells. The DTX or miRNA-142-3p alone can suppress malignant behavior and progression of breast cancer cells, but their combination elicits a synergistic effect that further enhances breast cancer inhibition. In summary, miRNA-142-3p transfection can be administered in conjunction with DTX therapy to enhance its cytotoxicity against breast cancer cells and prevent chemoresistance.