Elucidation of scandenolone as anti-cancer activity through impairment of the metabolic and signaling vulnerabilities in prostate cancer

Prostate cancer (PCa) is the most prevalent men's cancer in America and Western countries. No effective ther-apies are currently available for PCa aggressiveness, including castration-resistant progression (CRPC). This study aims at evaluation of the prospective efficacy and the molecular mechanism of scandenolone (SCA), a natural isoflavone, in PCa progression. SCA suppressed cell viability and progression and induced apoptosis in PCa cells. SCA inhibited the expression of lipogenesis and cholesterogenesis related key genes. Through inhi-bition of these metabolic genes, SCA decreased the levels of fatty acids, lipid droplets and cholesterols in PCa cells. Moreover, SCA enhanced the expression of antioxidant factors, including Nrf2, HO-1, catalase and SOD-1, and reduced the ROS levels in PCa cells. Substantially, SCA displayed the potential efficacy on CRPC tumors. This paper offers a new insight into the underlying molecular basis of SCA in PCa cells. By coordinated impairment of the metabolic and signaling vulnerabilities, including lipogenesis, cholesterogenesis, ROS and the AR/PSA axis, SCA could be applied as a novel and promising remedy to cure malignant PCa.

Automated summary

This study evaluates the potential efficacy and molecular mechanism of scandenolone (SCA), a natural isoflavone, in the progression of prostate cancer (PCa). The findings demonstrate that SCA can suppress cell viability and progression, induce apoptosis, and modulate metabolic and antioxidant factors in PCa cells. Furthermore, SCA shows potential efficacy against castration-resistant prostate cancer (CRPC) tumors.