Impact of genistein on androgen-independent PC3 prostate cancer cells

Purpose: This study evaluates genistein’s effects on cell survival, migration, apoptosis, reactive oxygen species (ROS) generation, and Manganese Superoxide Dismutase (MnSOD) expression in androgen-independent PC3 prostate cancer cells, providing insight into its potential as an adjuvant therapy for castration-resistant prostate cancer (CRPC). Materials and Methods: Cells were treated with vehicle only and 0.5, 2.5, 5, 10, and 50 µM genistein concentrations for 24 and 48 hours. Cell proliferation assay, wound healing assay, ROS measurement, apoptosis detection, and MnSOD protein expression analysis were performed. Results: The findings indicate a biphasic effect of genistein on PC3 cell survival. Lower to physiologically relevant concentrations (0.5–10 µM) exhibit a modest stimulatory effect, whereas a higher, pharmacologically achievable concentration (50 µM) leads to a time-dependent decline in survival and a significant restriction on migration. In vehicle-treated cells, 77% remained viable, with low early (3.65%) and late apoptosis (16.35%). Lower genistein concentrations (0.5–10 µM) caused a slight increase in apoptosis and a modest decline in viability. However, at 50 µM, only 18.7% of cells remained viable, while 74.25% underwent late apoptosis or cell death. Conclusion: These findings demonstrate that genistein, particularly at higher concentrations, inhibits androgen-independent PC3 cell growth through apoptosis induction, MnSOD regulation, and elevated oxidative stress.