Table 1 Different roles of NLRP3 inflammatory body in tumor occurrence and development.

Colorectal cancer

NLRP3 mediates STING signal transduction of macrophages, which promotes anti-tumor characteristics of 4-1BBL/4-1BBL-dependent NK cells and thus inhibits cancer development.

NLRP3 mediates IFN-g to activate tumor suppressor STAT1, which has a protective effect on tumorigenesis.

NLRP3 is activated by the crosstalk of mφ-CRC cells, which leads to faster migration of cancer cells.

Overproduction of 5-HT/TPH1 promotes cancer progression by enhancing inflammasome activation of NLRP3.

NLRP3 can promote the proliferation and metastasis by regulating epithelial–mesenchymal transition.

Gastric cancer

HP/M.hy leads to the activation of NLRP3 inflammatory corpuscle pathway and results in the migration and invasion of gastric cancer cells.

NLRP3 is combined with cyclin-D1 promoter, which promotes its transcription, enhances proliferation and GC occurrence.

CagA can promote the invasion and migration of gastric cancer cells by activating NLRP3 inflammatory corpuscles and generating ROS in cells.

Liver cancer

ROS mediate the inflammatory corpuscles of NLRP3 and inhibit the NF-kB signaling pathway in hepatocellular carcinoma cells, thus protecting tumor occurrence.

The expression of NLRP3 inflammatory corpuscles in liver cancer tissue decreased significantly and was negatively correlated with the pathological grade and clinical stage of liver cancer patients, so NLRP3 has a protective effect in cancer development.

Obesity-induced ER stress will lead to focal death of liver NLRP3 inflammatory corpuscles, thus mediating liver injury.

Pancreatic cancer

Platelet NLRP3 signal transduction promotes platelet activation and aggregation in PDA, thus promoting tumor growth.

NLRP3 deficiency inhibits the growth and progression of PDA tumor and cut down the occurrence of lung metastasis. On the contrary, the activation of NLRP3 enhanced the lung metastasis of pancreatic ductal adenocarcinoma.