NFKB1 and neoplasm: Taken together, these findings underline that the multicellular proinflammatory TME promotes HCT116 tumor cell progression, at least in part through NF-κB signaling pathways, and this pathway could be specifically inhibited by Calebin A. Thus, Calebin-A-mediated regulation of the NF-κB signaling pathway might exert an antitumorigenic effect in CRC tumor.