Ethyl Caffeate Suppresses Prostate Cancer Progression via PI3K/Akt Pathway Inhibition

Background The current therapeutic options for prostate cancer have limited efficacy and are plagued by significant drug resistance. Ethyl caffeate is a phenolic compound extracted from Ilex latifolia Thunb. Objective This study aimed to investigate the regulatory effects of Ethyl Caffeate (EC) on prostate cancer progression and elucidate the underlying mechanism by network pharmacology, in vivo and in vitro experimental analysis. Methods The DU145 and PC3 prostate cancer cell lines were used to evaluate the effects of EC on cell proliferation, migration, and cell cycle progression. A subcutaneous PC3 xenograft model was established in BALB/c-Nude mice to assess the biosafety and in vivo anti-tumor efficacy of EC. Network pharmacology and molecular docking were employed to predict potential molecular mechanisms underlying its effects on prostate cancer. Protein expression levels of key molecules in the PI3K/Akt pathway were detected by Western blot. Results EC inhibited the viability and migratory capacity of prostate cancer cells in a dose-dependent manner, and exerted anti-proliferative effects by inducing cell cycle arrest. In vivo experiments further demonstrated that EC suppressed tumor growth without significant toxicity. Based on network pharmacology and molecular docking predictions, and subsequent experimental validation, EC was shown to effectively inhibite the PI3K/Akt signaling pathway. Both in vitro and in vivo results confirmed that EC exerts its effects on prostate cancer through suppression of the PI3K/Akt pathway. Conclusion EC inhibits prostate cancer progression by silencing the PI3K/Akt pathway, suggesting its potential clinical value in the treatment of prostate cancer.