Abstract:
:Malignant pleural effusion (MPE) is a frequent metastatic manifestation of human cancers. While we previously identified KRAS mutations as molecular culprits of MPE formation, the underlying mechanism remained unknown. Here, we determine that non-canonical IKKα-RelB pathway activation of KRAS-mutant tumor cells mediates MPE development and this is fueled by host-provided interleukin IL-1β. Indeed, IKKα is required for the MPE-competence of KRAS-mutant tumor cells by activating non-canonical NF-κB signaling. IL-1β fuels addiction of mutant KRAS to IKKα resulting in increased CXCL1 secretion that fosters MPE-associated inflammation. Importantly, IL-1β-mediated NF-κB induction in KRAS-mutant tumor cells, as well as their resulting MPE-competence, can only be blocked by co-inhibition of both KRAS and IKKα, a strategy that overcomes drug resistance to individual treatments. Hence we show that mutant KRAS facilitates IKKα-mediated responsiveness of tumor cells to host IL-1β, thereby establishing a host-to-tumor signaling circuit that culminates in inflammatory MPE development and drug resistance.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Marazioti A,Lilis I,Vreka M,Apostolopoulou H,Kalogeropoulou A,Giopanou I,Giotopoulou GA,Krontira AC,Iliopoulou M,Kanellakis NI,Agalioti T,Giannou AD,Jones-Paris C,Iwakura Y,Kardamakis D,Blackwell TS,Taraviras S,Spella Mdoi
10.1038/s41467-018-03051-zsubject
Has Abstractpub_date
2018-02-14 00:00:00pages
672issue
1issn
2041-1723pii
10.1038/s41467-018-03051-zjournal_volume
9pub_type
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