Divergent functions of NLRP3 inflammasomes in cancer: a review

The cancer is a serious health problem, which is The cancer death rate (cancer mortality) is 158.3 per 100,000 men and women per year (based on 2013–2017 deaths). Both clinical and translational studies have demonstrated that chronic inflammation is associated with Cancer progression. However, the precise mechanisms of inflammasome, and the pathways that mediate this phenomenon are not fully characterized. One of the most recently identified signaling pathways, whose activation seems to affect many metabolic disorders, is the “inflammasome” a multiprotein complex composed of NLRP3 (nucleotide-binding domain and leucine-rich repeat protein 3), ASC (apoptosis associated speck-like protein containing a CARD), and procaspase-1. NLRP3 inflammasome activation leads to the processing and secretion of the proinflammatory cytokines interleukin-1β (IL-1β) and IL-18. The goal of this paper is to review new insights on the effects of the NLRP3 inflammasome activation in the complex mechanisms of crosstalk between different organs, for a better understanding of the role of chronic inflammation in cancer pathogenesis. We will provide here a perspective on the current research on NLRP3 inflammasome, which may represent an innovative therapeutic target to reverse the malignancy condition consequences of the inflammation. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12964-023-01235-9.