Prostate cancer progression::Sodium salicylate, the active metabolite of aspirin inhibits nuclear factor-kappa B (NFkB) pathway

Aim: Evidence from several studies suggests that nuclear factor-kappa B (NFκB) pathway is associated with cancer progression. Therefore, the inhibition of the NFκB pathway provides the focus for cancer management. Sodium salicylate, the active metabolite of aspirin has been shown to inhibit NFκB activation in prostate cell lines. In this study, we examine the role of NFκB pathway in PNT2 (normal prostate), DU145 (prostatic brain metastasis), PC3 (prostatic bone metastasis).Method: We exposed both normal prostate (PNT2) cells and prostate cancer (DU145, PC3) cell lines to sodium salicylate. NFκB activation in prostate cells was examined by ELISA (enzyme-linked immunosorbent assay) alongside controls. IKK an inhibitor of NFκB activation and tumour necrosis factor (TNF) a potent activator of NFκB were utilised as controls.Result: Our results suggest that sodium salicylate inhibits NFκB activation in prostate cancer cell lines. PC3 (the most aggressive cell line) showed a decreased level of NFκB activation after treatment with sodium salicylate. However, PNT2 and DU145 showed very little change in NFκB activation over the dose ranges applied.Conclusion: Our study provides further evidence that NFκB pathway is associated with prostate cancer progression as we observed NFκB activation and inhibition by sodium salicylate in all three prostatic cell lines