What’s known on the subject? and What does the study add? We found that resistin, a member of adipokine family, is expressed in human prostate cancers and induces prostate cancer cell proliferation through PI3K/Akt signaling pathways. We are studying the effect of resistin on other urogenital tract diseases besides prostate cancer, and the relationship between other adipokines and the urogenital tract diseases. OBJECTIVES • To determine whether resistin, a novel adipokine, induces prostate cancer cell proliferation. • To identify the mechanisms underlying the activation of prostate cancer cells by resistin. MATERIALS AND METHODS • Semi‐quantitative reverse transcriptase‐polymerase chain reaction and immunohistochemical staining were performed to investigate the intensity of prostate epithelial resistin expression. • Human full‐length resistin gene (RETN) was transfected into the PC‐3 cells using the pEGFP‐N1 vector to assess the effect of overexpression of resistin in prostate cancer cell line PC‐3. • Various concentrations of human recombinant protein resistin were added to the hormone‐insensitive prostate cancer cell lines PC‐3 and DU‐145 for 48 h, and cell proliferation was assessed by a water‐soluble tetrazolium salt assay. RESULTS • Human prostate cancer cell lines PC‐3 and DU‐145 were found to express the human resistin mRNA. • Resistin protein was strongly detected in high‐grade prostate cancer tissue, whereas BPH or low‐grade prostate cancer tissue revealed fainter expression of resistin. • Cell proliferation was stimulated by both the full‐length resistin gene overexpression and resistin treatment. • Akt phosphorylation occurred after addition of resistin to PC‐3 and DU‐145 cells. LY294002, a pharmacological inhibitor of phosphatidylinositol 3‐kinase (PI3K), significantly inhibited PC‐3 and DU‐145 cell proliferation after resistin treatment. CONCLUSIONS • Resistin is expressed in human prostate cancers. • Resistin induces prostate cancer cell proliferation through PI3K/Akt signalling pathways. • The proliferative effect of resistin on prostate cancer cells may account in part for prostate cancer progression.
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Kim et al. (2010) studied this question.
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