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Interleukin-1-Induced Promatrilysin Expression is Mediated by NF B-Regulated Synthesis of Interleukin-6 in the Prostate Carcinoma Cell Line , LNCaP 1

Previously, our laboratory showed that interleukin-1 ( IL-1 ) secreted by lipopolysaccharide-activated monocytes induces promatrilysin expression in the prostate carcinoma cell line, LNCaP. We now demonstrate that IL-1 induced promatrilysin expression is mediated by an indirect mechanism that requires nuclear factor Kappa B (NF B)-dependent synthesis of IL-6. Inhibition of protein synthesis with cyclohexamide blocked IL-1 mediated induction of matrilysin mRNA suggesting that synthesis of one or more additional factors is required for IL-1 induced promatrilysin protein expression. Blockage of NF B transactivation activity abrogated IL-1 induced promatrilysin expression to baseline levels suggesting that NF B transactivation activity is necessary. Inhibition of IL-6 activity attenuated IL-1 induced promatrilysin, but not NF B transactivation activity indicating that IL-6 acts downstream of NF B in potentiation of IL-1 -mediated promatrilysin expression. Inhibition of protein synthesis with cyclohexamide did not alter IL-6induced induction of matrilysin mRNA indicating that, contrary to the mechanism by which IL1 regulates promatrilysin expression, IL-6-mediated matrilysin mRNA expression does not require new protein synthesis. Transient transfection with dominant negative STAT3 inhibited IL-1 and IL-6 induced promatrilysin. These data provide evidence that NF Bmediated IL-6 synthesis is required for IL-1 induced promatrilysin expression, and IL-6 signaling through STAT3 plays a role in IL-1 induced promatrilysin expression. Neoplasia (2001) 3, 509–520.