Abstract
Inflammasomes are important intracellular multiprotein signaling complexes that modulate the activation of caspase-1 and induce levels of the proinflammatory cytokines interleukin-1β (IL-1β) and IL-18 in response to pathogenic microorganisms and molecules that originated from host proteins. Inflammasomes play contradictory roles in the development of inflammation-induced cancers. Based on several findings, inflammasomes can initiate and promote carcinogenesis. On the contrary, inflammasomes also exhibit anticancer effects by triggering pyroptosis and immunoregulatory functions. Herein, we review extant studies delving into different functions of inflammasomes in colorectal cancer development.
Highlights
Accepted: 29 July 2021Inflammasomes are critical regulators of inflammation by stimulating the secretion of proinflammatory cytokines after sensing harmful pathogens and endogenous danger signals by innate immune system receptors (pattern-recognition receptor (PRR)) [1,2]
Inflammasomes may have cancer model, Hu et al (2013) demonstrated that NLRP6 and ASC-deficient mice had an anticancer role. Multiple factors such as tumor microenvironments and gut a colitogenic gut microflora that induced exacerbated inflammation-induced colorectal microbiota could affect the exact role of an inflammasome
Colon after dextran sodium sulfate (DSS) administration, and these mice were more susceptible to DSS-induced coliSeveral studies have shown that NLRP3/NLRC4-deficient mice were more susceptible to tis such as colorectal tumorigenesis
Summary
Inflammasomes are critical regulators of inflammation by stimulating the secretion of proinflammatory cytokines after sensing harmful pathogens and endogenous danger signals by innate immune system receptors (pattern-recognition receptor (PRR)) [1,2]. In addition to the activation of caspases and proinflammatory cytokines, the activation of inflammasomes leads to the programmed cell death pyroptosis as a gasdermindependent form of cell death [12] This is the term used to describe the release of cytoplasmic components in the extracellular space by the creation of membrane pores [13]. Non-inflammasome-forming PRRs like TLRs and NOD1/NOD2 are important in pyroptosis These receptors, via the activation of NF-κB and MAPK-signaling pathways, will upregulate inflammatory cytokine expressions (IFN α/β,TNF, IL-12 and IL-6) [22,23]. The influx of potassium ions upon membrane permeabilization stimulates NLRP3 activation, resulting in NLRP3 inflammasome formation and the activation of caspase-1 These processes promote GSDMD cleaving and improve the maturation and release of the proinflammatory cytokines [17]. After discussing the main function of inflammasomes, we discuss the association between inflammasome components and intestinal carcinogenesis
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