Naringenin Inhibits Cellular Proliferation, Arrests Cell Cycle and Induces Pro-Apoptotic Autophagy in MCF-7 Breast Cancer Cells.

The global incidence of breast cancer has significantly increased, highlighting the need for novel therapeutic strategies. Current treatment options are often limited by drug resistance and adverse effects, necessitating the exploration of alternative compounds. Naringenin, a naturally occurring flavonoid in citrus fruits, exhibits antimicrobial, anti-atherogenic, hepatoprotective, anti-inflammatory, and anticancer properties. This study evaluates the potential of naringenin as an inhibitor of breast cancer cell proliferation. MCF-7 breast cancer cells were used as a model system to assess the anti-proliferative effects of naringenin. Cell viability was evaluated using MTT and colony formation assays, while cell migration was analysed via wound healing assay. Flow cytometry and western blotting were performed to examine cell cycle arrest and apoptosis, and autophagy was assessed through western blotting and confocal microscopy. Naringenin inhibited cellular proliferation in a dose-dependent manner by arresting cells in the S-phase of the cell cycle. It significantly reduced cellular migration and increased early and late apoptosis. Autophagy induction was confirmed by elevated LC3-II expression, p62 degradation, and LC3-II-LAMP1 co-localization. Additionally, C-PARP expression was reduced when cells were co-treated with naringenin and 3-methyladenine (3-MA), indicating pro-apoptotic autophagy. This study demonstrates the anti-migratory and anti-proliferative effects of naringenin and its ability to induce pro-apoptotic autophagy in human breast cancer cells, suggesting its potential as a therapeutic agent.