Ryan SL, Beard S, Barr MP, et al. - Researchers sought to assess the role of inflammatory mediators in cisplatin-resistance in non-small cell lung cancer (NSCLC). They investigated an isogenic model of cisplatin-resistant NSCLC for inflammatory mediator, NF-κB, and its associated pathways using age-matched parental (PT) and corresponding cisplatin-resistant (CisR) sublines. Proteomic analysis identified that CisR cells vs PT cells had dysregulated NF-κB responsive targets, with increased NF-κB expression identified in four out of the five NSCLC sub-types examined (CisR vs PT). Reduction in NF-κB expression was noted with DHMEQ (an NF-κB small molecule inhibitor) treatment in the presence of cisplatin, and further, the treatment re-sensitized CisR cells to the cytotoxic effects of the drug. Findings thereby support NF-ĸB as a potential therapeutic target in cisplatin-resistant NSCLC. Furthermore, chemo-resistant cells re-sensitized to cisplatin treatment following inhibition of NF-ĸB using DHMEQ.