<p>Breast cancer poses significant therapeutic challenges, necessitating the identification of novel molecular targets for effective treatment. This study explores the tumor-suppressive role of miR-593-3p and its regulatory interaction with TIMM17A in breast cancer. Expression analysis revealed a marked downregulation of miR-593-3p in breast cancer cell lines compared to normal mammary epithelial cells. Functional assays demonstrated that miR-593-3p overexpression in MDA-MB-231 cells inhibited proliferation, suppressed colony formation, and induced apoptosis, as confirmed by CCK-8 and Annexin V/PI assays. Bioinformatics predictions and dual luciferase reporter assays identified TIMM17A as a direct target of miR-593-3p. Western blot analysis showed that miR-593-3p overexpression considerably reduced TIMM17A levels. Furthermore, TIMM17A was upregulated in breast cancer tissues and correlated with poor clinical outcomes. Knockdown of TIMM17A suppressed cell growth and invasion, while its overexpression counteracted the inhibitory effects of miR-593-3p. Transwell assays further demonstrated that miR-593-3p reduced the invasive potential of MDA-MB-231 cells by regulating TIMM17A These findings indicate that miR-593-3p functions as a tumor suppressor by targeting TIMM17A, influencing both proliferative and invasive properties of breast cancer cells. The identification of this regulatory axis suggests that miR-593-3p could serve as a promising therapeutic target for breast cancer treatment.</p> Graphical Abstract <p></p>