Title:Inflammasome, Inflammation and Cancer: An Interrelated Pathobiological Triad
Volume: 16
Issue: 3
Author(s): Gyorgyi Muzes and Ferenc Sipos
Affiliation:
Keywords:
Cancer, caspase-1, inflammation, inflammasome, pro-inflammatory cytokines, pyroptosis.
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.
