Tumour-promoting
inflammation is a critical hallmark in
cancer development, and
inflammasomes are well-known 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-1β 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.