Colorectal Cancer and NLRP-Current Knowledge

Abstract

Inflammasomes activated by different stimuli in colorectal cancer show dual effect on cancer’s destiny. Activation of caspase-1 results in maturation of IL-1β and IL-18. IL-1β suppresses NK and T cells activity against tumor, induces expression of metastatic genes and stimulates the production of proinflammatory leukines, but it also enhances NK cell–mediated death of colon carcinoma cells. IL-18 promoter polymorphisms in humans increase risk for colorectal cancers. One variant of NLRP3 gene in human is connected with increased susceptibility to colorectal cancer. Expression levels of NLRP1, NLRP3, NLRC4 were significantly reduced in human CRC compared with healthy controls. Nlrp3 −/−mice exhibited increased colorectal cancer and metastasis in liver. NLRP3 have an important role in the Epithelial-Mesenchymal Transition (EMT) of colorectal cancer cells, which is necessary for migration and invasion. Absence of NLRP3 in colorectal carcinoma cells diminishes tumor cells migration and invasion.