Raloxifene suppresses growth and promotes intrinsic apoptotic signaling in C6 glioma cells.

Glioblastoma (GBM), the most common malignant brain tumor, remains highly resistant to current standard treatments, highlighting the urgent need for novel treatment strategies. Epidemiological evidence shows a lower incidence rate of GBM in women than in men, suggesting a potential protective role of estrogen. Given that GBM cells disturb cell cycle regulation through uncontrolled proliferation, targeting apoptotic pathways has emerged as a promising therapeutic approach. Raloxifene (RAL), a selective estrogen receptor modulator (SERM), has repeatedly demonstrated anticancer potential. In this study, we investigated whether RAL could induce apoptosis in GBM cells. Using rat C6 cells, we evaluated RAL's effects on cell viability, apoptosis induction, cell cycle progression, migration capacity, and colony formation, as well as on the gene and protein expression profiles of apoptosis-related signaling pathways. Our findings show that RAL significantly induces apoptosis and suppresses cell growth in a concentration- and time-dependent pattern compared to the vehicle control (0.1% DMSO). These findings would position RAL as a promising candidate for GBM therapy, warranting further investigation into its translational potential.