Fig. 4

Schematic of NLRP3 inflammasome involvement in GI tract cancers. Accumulating evidences suggest that NLRP3 inflammasome activation underpins the onset of several cancers in the gastrointestinal tract. Environmental nitrosamines-mediated NLRP3 activation has been hypothesized to be involved in the EC. NLRP3 activation functions as immunosuppressor in HCC modulating the tumoricidal activity of NK cell. Helicobacter bilis (H. bilis) and Helicobacter hepaticus (H. hepaticus) induce CCA via NLRP3 inflammasome, whereas high 5-HT level and Porphyromonas gingivalis colonization promote CRC. Expression of lncRNA XLOC_000647 prevents PDA by dampening NLRP3 activation. H. pylori and M. hyorhinis trigger GC upon NLRP3 activation. Finally, NLRP3 activation fosters the phosphorylation of AKT, ERK and cAMP signaling pathway which supports GBC onset