Structuring Inflammasome-Epigenome: Phenotypic Axis in Gynecological Cancers

Inflammasomes are made up of sensor proteins, caspase domain having adaptor protein, and caspase-1 aka pro-inflammatory caspase present in the cytoplasmic membrane of the cell. They get activated in the presence of pathogen infection or a stress condition leading to the stimulation of IL-1β and IL-18, i.e., pro-inflammatory cytokines. These inflammasomes are activated through sensing pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs), involving a variety of immune system disorders. The interaction between the immune system and cancer recognized the importance of inflammasomes in various disorders of cancer. Out of all the inflammasomes, NLRP3 is the most important one and is commonly associated with tumorigenesis and involved in tumor progression. To control inflammasomes, epigenetic regulation and autophagic modulation are done. Epigenetic regulation occurs through post-translational modification via methylation, modification of histone, and also, expression of noncoding RNA. The upregulation and downstream of inflammasomes determine the development of pathologies with a different outcome. Additionally, autophagy modulation known as homeostasis controller act on inflammasomes-mediated tumor and try to maintain homeostasis condition in them to remove risk factor involved in cancer development. As NLRP3 inflammasomes play a variety of roles in tumorigenesis, they can be deployed as a potential anticancer drug target. The main focus of this review will be to summarize the role of inflammasomes in cancer through the expression of cytokines IL-1β and IL-18 and the effect of epigenetic and autophagic modulation on controlling inflammasomes. There is a need for further research on inflammasome significance in the cancer domain as the results are contrasting.