Eriocitrin promotes apoptosis and inhibits invasion and proliferation of androgen-independent prostate cancer via the PI3K/AKT/mTOR pathway

Androgen-independent prostate cancer represents a highly aggressive malignancy with limited therapeutic options, during which the hyperactivation of the PI3K/AKT/mTOR signaling pathway plays an important role in disease progression, presenting a critical target for therapeutic intervention. Eriocitrin, a natural flavonoid compound, has exhibited potential bioactivities; however, its specific anti-tumor efficacy and underlying mechanisms in prostate cancer remain poorly characterized. Our initial screening across multiple prostate cancer cell lines revealed that androgen-independent DU145 cells were particularly sensitive to Eriocitrin. Subsequent investigations demonstrated that Eriocitrin significantly suppressed DU145 cell proliferation and induced apoptosis in a concentration-dependent manner. Furthermore, Eriocitrin effectively impaired cell migration and invasion, which was mechanistically driven by the reversal of the epithelial-mesenchymal transition (EMT) process, notably through the upregulation of E-cadherin. Molecular analyses revealed that Eriocitrin exerted these anti-tumor effects by inhibiting the activation of the PI3K/AKT/mTOR signaling cascade. Taken together, this in vitro study provides novel preclinical evidence that Eriocitrin restrains the aggressive phenotypes of androgen-independent prostate cancer via the PI3K/AKT/mTOR axis. These findings highlight Eriocitrin as a biologically active plant-derived compound that warrants further comprehensive in vivo and pharmacokinetic investigations to determine its true therapeutic potential.