Abstract
Cancer represents a major health problem worldwide, therefore on the basis of current research results constantly more effective therapeutic strategies are expected. Chronic, unchecked inflammation has widely been suggested to trigger carcinogenesis. The innate immune system ensures a first line host defense in which the inflammasome is essential maintaining a delicate balance betweeen pro- and anti-inflammatory signals in order to generate an appropriate immune response without harming the host. Studies have revealed a remarkable, but contradictory link of host inflammatory responses to tumorigenesis. Indeed, activation of the multiprotein complex inflammasome by danger signals seems to play diverse and sometimes conflicting, suppressive or stimulatory role in cancer development and progression with a significant context-dependency. The pleitropic inflammasomes may act at cellautonomous level to eliminate malignant cells via the programmed cell death type of inflammatory pyroptosis, but on the contrary, may favor the production of gowth and trophic factors for tumor cells and their microenvironment. Further, upon caspase-1 activation the inflammasome can provoke sterile inflammation, and thus facilitate carcinogenesis, though in antigen-presenting cells it can elicit anti-tumor immune responses. Clarifying the exact, context-specific impact of inflammasomes on tumorigenesis represents a new research area with the potential to introduce promising novel targets for cancer therapeutics.
Keywords: Cancer, caspase-1, inflammation, inflammasome, pro-inflammatory cytokines, pyroptosis.
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