Inflammasome as a promising therapeutic target for cancer

Abstract

Inflammasomes are the major mechanistic complexes that include members of the NOD-like receptor (NLRs) or AIM2-like receptors (ALRs) families, which are affiliated with the innate immune system. Once NLRs or ALRs are activated by pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patterns (DAMPs), the caspase-1 or -11 is activated by binding with NLRs or ALRs via its own unique cytosolic domains. As a result, caspase-1 or -11 enhances the production of IL-1β and IL-18, which results in inflammation via the recruitment of immune cells, such as macrophages, and the promotion of programmed cell death mechanisms such as pyroptosis. In addition, the consistent cascades of inflammasomes would precede both minor and severe autoimmune diseases and cancers. The clinical relevance of inflammasomes in multiple forms of cancer highlights their therapeutic promise as molecular targets. To closely analyze the physiological roles of inflammasomes in cancers, here, we describe the fundamental knowledge regarding the current issues of inflammasomes in relevant cancers, and discuss possible therapeutic values in targeting these inflammasomes for the prevention and treatment of cancer.

Keywords: Anakinra (PubChem CID: 90470007); BAY-11-7082 (PubChem CID: 5353431); Cancer; Glyburide (PubChem CID: 3488); Hydroxybutyrate (PubChem CID: 441); Inflammasome; Inhibitors; MCC950 (PubChem CID: 9910393); N-acetyl Cysteine (PubChem CID: 12035); NLRP; Ritonavir (PubChem CID: 392622); Thalidomide (PubChem CID: 5426); Therapeutics; VX-740 (PubChem CID: 153270); VX-765 (PubChem CID: 11398092).