A newly synthesized compound induces apoptosis in prostate cancer cells by targeting mitochondrial dysfunction and the TP53/BCL-2/SEMA3 pathways.

Recent investigations have emphasized the therapeutic potential of thiazole derivatives in oncology. In this study, the novel compound 2-[(4,5-dihydrothiazol-2-yl)thio]-N-(4-methylthiazol-2-yl)acetamide was evaluated for its cytotoxic and mechanistic effects on PC-3 prostate cancer cells. Cell viability decreased significantly after treatment (∗∗∗∗p ≤ 0.0001), and HEK-293 cells showed relative resistance at lower doses. Annexin V/PI flow cytometry revealed a dose-dependent increase in apoptosis, most pronounced at 88 μM (∗∗∗∗p < 0.0001), and JC-1 assays confirmed membrane depolarization (∗∗∗∗p < 0.0001). RT-qPCR analysis revealed significant downregulation of PSA and c-MYC (∗∗∗∗p < 0.0001) with a mild increase in TP53 expression. ELISA-based protein quantification showed elevated Caspase-3 and a biphasic modulation of Cytochrome-c, supporting activation of intrinsic apoptosis. GPX4 levels remained largely unchanged except at 128 μM, and SEMA3A expression was not significantly affected. Among inflammatory cytokines, TNF-α levels increased dose-dependently (∗∗∗∗p < 0.0001), while IL-6 and IL-10 showed no significant alterations. Collectively, These findings indicate that the synthesized thiazole compound exerts selective cytotoxicity toward prostate cancer cells via mitochondria-mediated apoptosis and inflammatory signaling modulation.