Inflammasomes in cancer: Effect of epigenetic and autophagic modulations

Tumour-promoting inflammation is a critical hallmark in cancer development, and inflammasomes are wellknown regulators of inflammatory processes within the tumour microenvironment. Different inflammasome components along with the adaptor, apoptosis-associated speck-like protein containing caspase activation and recruitment domain (ASC), and the effector, caspase-1, have a significant influence on tumorigenesis but in a tissue-specific and stage-dependent manner. The downstream products of inflammasome activation, that is the proinflammatory cytokines such as IL-1 beta and IL-18, regulate tissue homeostasis and induce antitumour immune responses, but in contrast, they can also favour cancer growth and proliferation by directing various oncogenic signalling pathways in cancer cells. Moreover, different epigenetic mechanisms, including DNA methylation, histone modification and noncoding RNAs, control inflammasomes and their components by regulating gene expression during cancer progression. Furthermore, autophagy, a master controller of cellular homeostasis, targets inflammasome-induced carcinogenesis by maintaining cellular homeostasis and removing potential cancer risk factors that promote inflammasome activation in support of tumorigenesis. Here, in this review, we summarize the effect of inflammasome activation in cancers and discuss the role of epigenetic and autophagic regulatory mechanisms in controlling inflammasomes. A proper understanding of the interactions among these key processes will be useful for developing novel therapeutic regimens for targeting inflammasomes in cancer.

Automated summary

Inflammasomes play a critical role in tumor development, and their components have significant effects on tumorigenesis in a tissue-specific and stage-dependent manner. The proinflammatory cytokines produced by inflammasome activation can regulate tissue homeostasis and induce antitumor immune responses, but they can also promote cancer growth and proliferation by directing oncogenic signaling pathways in cancer cells. Epigenetic mechanisms and autophagy control inflammasome activation and contribute to cancer development.