Amarogentin Inhibits Cell Viability and Promotes Apoptosis in Breast Cancer MDA-MB-231 Cells via Increasing Oxidative Stress and Inhibiting PI3K/AKT/mTOR Pathway

Background Breast cancer is the most common cancer type in women globally, constituting a substantial portion of all documented female malignancies. It is the second major cause of cancer-associated mortality in women, with over one million new diagnoses each year. Purpose The present work evaluated the anti-cancer activity of amarogentin by assessing its growth-inhibition and apoptosis-triggering capabilities against breast cancer cells. Materials and Methods The cytotoxic effects of amarogentin at various dosages on MDA-MB-231 cells were evaluated using the MTT test. The incidences of apoptosis in amarogentin-induced cells were evaluated using a dual staining technique. The concentrations of oxidative stress markers and PI3K/AKT/mTOR proteins were evaluated in amarogentin-treated cells utilizing kits. Results The current findings demonstrate that the MDA-MB-231 cell viability was diminished after treatment with diverse dosages of amarogentin. The amarogentin treatment significantly enhanced apoptotic incidences in MDA-MB-231 cells, as seen by the dual staining assay results. The amarogentin treatment elevated thiobarbituric acid reactive substances level and subsequently diminished antioxidants in the MDA-MB-231 cells. Furthermore, amarogentin suppressed PI3K/AKT/mTOR proteins in the breast cancer cells. Conclusion The current findings indicate that amarogentin treatment significantly reduces cell viability and promotes oxidative stress-dependent apoptosis in breast cancer cells. Therefore, it has the potential to serve as an anti-cancer candidate for breast cancer treatment.