The present study aimed to understand the roles of hepcidin and iron metabolism in the onset of prostate cancer. The prostate cancer LNCap, PC3 and DU145 cell lines were transfected with small interfering RNA (siRNA) targeting hepcidin to knockdown hepcidin expression in LNCap, PC3 and DU145 cells. The expression levels of hepcidin in prostate cancer and normal prostate RWPE-1cells were detected by western blot analysis. Exogenous hepcidin was added into the hepcidin-silenced cell lines. Intracellular iron levels were detected using a fluorescence assay, and the proliferative and migratory capacities of cells were detected using the MTT and wound-healing assays, respectively. The apoptotic rate was measured using flow cytometry, and changes in the expression of the iron-export protein ferroportin on the cell membrane were detected by western blot analysis. Hepcidin expression in prostate cancer cells was significantly higher than that of normal prostate cells (P<0.05). Furthermore, the iron levels of hepcidin-silenced cells (hepcidin^-ve groups) were significantly lower than those in the cells treated with exogenous hepcidin (hepcidin^+ve groups) (P<0.05). The proliferative capacity of the hepcidin^+ve cells significantly exceeded those of the hepcidin^-ve groups (P<0.05) and increased over time. In the wound-healing assay, the number of hepcidin^+ve cells present within the scratch sites increased compared with hepcidin^-ve cells, indicating a higher migration rate. Additionally, the expression of ferroportin in the hepcidin^-ve groups significantly exceeded that in the hepcidin^+ve groups (P<0.05). Hepcidin is involved in the onset of prostate cancer, most likely by reducing ferroportin expression and increasing intracellular iron levels to enhance the proliferation, migration and anti-apoptotic capacities of cancer cells.

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