Fig. 1.

Regulation and role of AIM2 in cancer development. AIM2 expression is induced in a variety of cell types by Type I IFNs or IL-1β-induced signaling. Increased levels of POP3 or IFI16 inhibit activation of the AIM2 inflammasome. Activation of AIM2 inflammasome in macrophages and dendritic cells leads to inflammatory cell death by pyroptosis. However, pyroptosis suppresses the expression of IFN-β and Type I IFN response. IFN-induced IFI16 levels potentiate cellular senescence-associated permanent cell cycle arrest in cells through activation of the p53 and pRb pathway. Increased production of IL-1β inhibits p53-mediated functions. Accumulation of senescent cells leads to senescent-associated secretory phenotype and inflammation. Proliferation of epithelial cells in inflammatory microenvironment results in accumulation of mutations and neoplastic transformation