Table 1.
Role of inflammasomes in tumorigenesis
| Inflammasome compartments | Pro- or anti-tumorigenesis | Type of tumors | Outcomes | References |
|---|---|---|---|---|
| NLRP1 | Pro-tumorigenesis (mutation) | Palmoplantar carcinoma | Gain-of-function mutations in NLRP1 are associated with multiple self-healing palmoplantar carcinoma | [59] |
| Pro-tumorigenesis (mutation) | Melanoma | NLRP1 variant rs12150220 is associated with higher risk of melanoma | [125] | |
| NLRP3 | Pro-tumorigenesis (mutation) | Melanoma | NLRP3 variant rs35829419 is associated with higher risk of melanoma | [125] |
| Pro-tumorigenesis (mutation) | Gastric cancer | NLRP3 variants rs10754558 and rs4612666 are significantly associated with gastric cancer | [126] | |
| Pro-tumorigenesis (mutation) | Pancreatic cancer | NLRP3 mutation Q705K is associated with pancreatic cancer | [127] | |
| Pro-tumorigenesis | Sarcoma | NLRP3 knockout protects mice from methylcholanthrene-induced sarcoma | [132] | |
| Pro-tumorigenesis | Papilloma | NLRP3-deficient mice are resistant to carcinogenesis-induced papilloma | [296] | |
| Pro-tumorigenesis | Squamous cell carcinoma | NLRP3 knockout protects mice from 4-NQO-induced squamous cell carcinoma | [133] | |
| Anti-tumorigenesis | Liver cancer | NLRP3 is downregulated during liver cancer development | [134] | |
| Anti-tumorigenesis | Colon cancer | NLRP3-deficient mice are susceptible to colitis-associated cancer | [137] | |
| Anti-tumorigenesis | Colon cancer | NLRP3 knockout increases colitis and colitis-associated cancer | [136] | |
| NLRC4 | Anti-tumorigenesis | Colon cancer | NLRC4-deficient mice show enhanced tumor formation | [141] |
| Pyrin | Anti-tumorigenesis | Colon cancer | Pyrin knockout increases colitis and tumorigenesis through promoting intestinal barrier integrity | [138] |
| ASC | Pro-tumorigenesis | Gastric cancer | ASC knockout suppresses spontaneous gastric cancer | [129] |
| Pro-tumorigenesis | Cecal cancer | ASC knockout suppresses spontaneous cecal cancer | [130] | |
| Pro-tumorigenesis | Skin cancer | Conditional knockout of ASC in myeloid cells reduces chemical-induced skin cancer | [143] | |
| Anti-tumorigenesis | Squamous cell carcinoma | ASC knockout promotes tumorigenesis through decreasing anti-tumor immunity | [135] | |
| Anti-tumorigenesis | Skin cancer | Conditional knockout of ASC in keratinocytes augments chemical-induced skin cancer | [143] | |
| Caspase-1 | Pro-tumorigenesis | Cecal cancer | Caspase-1 inhibitor suppresses spontaneous cecal cancer | [130] |
| Pro-tumorigenesis | Squamous cell carcinoma | Caspase-1 knockout protects mice from 4-NQO-induced squamous cell carcinoma | [133] | |
| Anti-tumorigenesis | Squamous cell carcinoma | Caspase-1 knockout promotes tumorigenesis through decreasing anti-tumor immunity | [135] | |
| Anti-tumorigenesis | Colon cancer | Caspase-1-deficient mice show enhanced tumor formation | [141] | |
| Caspase-11 | Anti-tumorigenesis | Colon cancer | Caspase-11 knockout mice are more susceptible to colitis-associated cancer | [139] |
| IL-1α | Anti-tumorigenesis | Breast cancer | IL-1α knockout mice show higher tumor burden and elevated death rate | [140] |
| IL-1β | Pro-tumorigenesis | Gastric cancer | Overexpression of IL-1β causes spontaneous gastric cancer | [131] |
| Pro-tumorigenesis | Lung cancer | Anti-inflammatory therapy by canakinumab reduced lung cancer incidence | [284] | |
| IL-18 | Pro-tumorigenesis (mutation) | Lymphoma | IL-18 variant rs1946518 is associated with higher risk of lymphoma | [128] |
| IL-1R1 | Anti-tumorigenesis | Breast cancer | IL-1R1 knockout mice show higher tumor burden and elevated death rate | [140] |