Erianin suppresses prostate cancer progression and attenuates STAT3 signaling

Abstract

Prostate cancer is one of the most prevalent malignancies in men, but current therapeutic strategies are often limited by suboptimal efficacy and the emergence of drug resistance. Cell proliferation, migration, and invasion were assessed using CCK-8, colony formation, wound healing, and Transwell assays in PC-3, 22RV1, and RM-1 cells. Network pharmacology and molecular docking were used to identify candidate targets, and the effects of erianin on target were subsequently examined by western blot analysis. In vivo antitumor activity was evaluated in C57BL/6N mice bearing RM-1 tumors. Liver and kidney functions were assessed using biochemical kits, and histopathological changes in major organs were examined by H&E staining. Among the 48 compounds screened, erianin showed the most potent anti-prostate cancer activity. Further assays showed that erianin reduced colony formation, wound closure, and Transwell invaded-cell counts. In vivo , erianin markedly suppressed tumor growth, with the 20 mg/kg dose exhibiting the strongest effect. Network pharmacology and molecular docking predicted STAT3 as a candidate target of erianin, while further analysis indicated that erianin inhibited STAT3 phosphorylation and downregulated its downstream effectors including c-Myc and MMP-9. Safety evaluation revealed that erianin caused only a mild elevation in serum alanine aminotransferase (ALT) without significant histopathological alterations in major organs. These findings demonstrate that erianin exerts potent anti-prostate cancer activity and that these effects are accompanied by reduced STAT3 signaling. Further functional and target-engagement studies are required to determine whether STAT3 inhibition is necessary for erianin.