miR-223-3p Targets <i>KIF4A</i> and Promotes the Oxidative Stress-Mediated Apoptosis of Breast Cancer Cells

<b><i>Background:</i></b> The abnormal expression of kinase family member 4A (<i>KIF4A</i>) is linked to breast cancer progression, with numerous miRNAs exhibiting abnormal expression. Thus, there is an urgent need to investigate the mechanisms of action of miRNAs and their target genes for the diagnosis and treatment of breast cancer. <b><i>Materials and Methods:</i></b> A bioinformatics analysis was conducted to screen for <i>KIF4A</i>, a key gene involved in oxidative stress in breast cancer cells. Using CCK8, EdU, cell healing, and Transwell assays, the knockdown of <i>KIF4A</i> was found to effectively inhibit the proliferation, migration, and invasion of breast cancer cells. Dual-luciferase assay and Western blotting confirmed that miR-223-3p targets and regulates <i>KIF4A</i> expression. The impact of miR-223-3p and <i>KIF4A</i> on oxidative stress in breast cancer cells was assessed through reactive oxygen species (ROS), superoxide dismutase (SOD), and malondialdehyde (MDA) measurements. Flow cytometry was used to evaluate tumor cell apoptosis. <b><i>Results:</i></b> Our results suggest that <i>KIF4A</i> is a downstream target of miR-223-3p. miR-223-3p inhibits the proliferation and invasion of breast cancer cells by directly targeting and downregulating <i>KIF4A</i>. Importantly, we found that miR-223-3p and <i>KIF4A</i> play important roles in regulating oxidative stress and apoptosis in breast cancer cells. Specifically, miR-223-3p promoted apoptosis by inhibiting the expression of <i>KIF4A</i>, increasing the accumulation level of ROS and MDA, and inhibiting the activity of SOD while <i>KIF4A</i> was overexpressed.