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 mu M 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 mu M) exhibit a modest stimulatory effect, whereas a higher, pharmacologically achievable concentration (50 mu M) 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 mu M) caused a slight increase in apoptosis and a modest decline in viability. However, at 50 mu M, 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.