Abstract
Prostate cancer remains one of the most prevalent malignancies among men worldwide, highlighting the need for novel therapeutic strategies with improved safety and efficacy profiles. Dietary polyphenols derived from Camellia sinensis (tea) have attracted considerable attention due to their antioxidant and anticancer properties. The present study evaluated the therapeutic potential of Camellia sinensis polyphenols in human prostate cancer cells by investigating their effects on cell viability, oxidative stress, apoptosis-related genes, antioxidant defense pathways, and cell-cycle regulation. Human prostate cancer cell lines PC-3 (androgen-independent) and LNCaP (androgen-dependent) were treated with polyphenol concentrations ranging from 10 to 100 µg/mL for 24 and 48 h. Polyphenol treatment induced a dose- and time-dependent reduction in cell viability. At 100 µg/mL for 48 h, cell viability decreased by approximately 72% in PC-3 cells and 80% in LNCaP cells, with calculated IC₅₀ values of 41.2 µg/mL and 29.5 µg/mL, respectively. Intracellular reactive oxygen species (ROS) levels were significantly reduced, reaching 70.1% suppression in PC-3 cells and 73.2% in LNCaP cells at the highest concentration. Quantitative real-time PCR analysis revealed marked upregulation of pro-apoptotic genes, with BAX expression increased by 3.4-fold in PC-3 cells and 3.9-fold in LNCaP cells, and CASP3 increased by up to 2.8-fold and 3.2-fold, respectively. Conversely, the anti-apoptotic gene BCL2 was downregulated by 64–68%, resulting in a substantial increase in the BAX/BCL2 ratio. Polyphenol treatment also enhanced antioxidant defense, with Nrf2 expression elevated by 2.2-fold, SOD1 by up to 2.4-fold, and CAT by up to 2.1-fold. Additionally, expression of the proliferation-associated gene CCND1 was suppressed by 67–70%, consistent with reduced cell growth. These findings demonstrate that Camellia sinensis polyphenols exert potent anticancer effects in prostate cancer cells through coordinated regulation of oxidative stress, apoptosis, and cell-cycle progression, supporting their potential role as adjunct agents in prostate cancer management.