Established and novel NF-κB inhibitors lead to downregulation of TLR3 and the proliferation and cytokine secretion in HNSCC.

摘要: The transcriptional activation of NF-κB signalling has been identified as a major pathway involved in inflammation and tumor aggressiveness number human cancers. Here we identify the impact miscellaneous known so far unknown inhibitors originating from different drug classes on function proliferation HNSCC. In detail: HNSCC cell lines were exposed to Acetylsalicylic Acid (ASA), Celecoxib, Dexamethasone, Curcumin EPs 7630. Our interest was detect upstream alterations after applying inhibiting substances. inhibition leads an regulation Toll-like-receptor 3 (TLR3), predominant receptor driving expansion. We find marked downregulation TLR3 IKK complex, documenting responses by every agent tested. second step further analyse proliferation, cytokine production expression downstream proteins such cyclin D1 c-Myc. data demonstrate decreased response incubation with aforementioned agents. Modulation is accompanied altered profiles IL-6 IL-8 which are relevant cytokines progression. Proto-oncogenes c-myc downregulated all Apart interplay TLR3, substantiated 7630 new natural inhibitor.