MicroRNA-195-5p Targets MYB to Regulate Proliferation and Malignant Metastasis in Triple-Negative Breast Cancer via PI3K/AKT/mTOR Signaling.

Objective: To investigate the effect of microRNA-195-5p (miRNA-195-5p) on proliferation and malignant metastasis in triple-negative breast cancer (TNBC) cells and its underlying mechanism. Methods: Expression levels of miRNA-195-5p and MYB were determined by quantitative real-time PCR (RT-qPCR) in TNBC cells (MDA-MB-231 and BT-549) and normal human mammary epithelial cells (MCF-10A). Cell proliferation was assessed via CCK-8 assays after miRNA-195-5p overexpression or knockdown in MDA-MB-231 cells. Transwell assays evaluated cellular invasion and migration. Western blotting analyzed impacts on the PI3K/AKT/mTOR pathway. Targeting of MYB by miRNA-195-5p was confirmed using TargetScan prediction and dual-luciferase reporter assays. RT-qPCR measured MYB expression upon miRNA-195-5p modulation. Rescue experiments (co-overexpression of MYB and miRNA-195-5p) further assessed proliferation and PI3K/AKT/mTOR signaling via CCK-8 and Western blotting. Results: Compared to MCF-10A cells, miRNA-195-5p expression was significantly downregulated (p < 0.01), while MYB was markedly upregulated (p < 0.001) in TNBC cells. Overexpression of miRNA-195-5p inhibited MDA-MB-231 proliferation, invasion, and migration; conversely, its knockdown promoted these phenotypes. MiRNA-195-5p directly targeted and negatively regulated MYB. MYB overexpression activated the PI3K/AKT/mTOR pathway, enhancing cell proliferation. Rescue experiments indicated that MYB upregulation counteracted the tumor-suppressive effects of miRNA-195-5p and reactivated PI3K/AKT/mTOR signaling. Conclusion: miRNA-195-5p suppresses proliferation and metastasis in TNBC by targeting MYB and inhibiting the PI3K/AKT/mTOR pathway.