Abstract
Chronic inflammation contributes to the development and progression of various tumors. Especially where the inflammation is mediated by cells of the innate immune system, the NLRP3 inflammasome plays an important role, as it senses and responds to a variety of exogenous and endogenous pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs). The NLRP3 inflammasome is responsible for the maturation and secretion of the proinflammatory cytokines interleukin-1β (IL-1β) and IL-18 and for the induction of a type of inflammatory cell death known as pyroptosis. Overactivation of the NLRP3 inflammasome can be a driver of various diseases. Since leukemia is known to be an inflammation-driven cancer and IL-1β is produced in elevated levels by leukemic cells, research on NLRP3 in the context of leukemia has increased in recent years. In this review, we summarize the current knowledge on leukemia-promoting inflammation and, in particular, the role of the NLRP3 inflammasome in different types of leukemia. Furthermore, we examine a connection between NLRP3, autophagy and leukemia.
Highlights
The genetic polymorphisms and expression profiles of NOD-like receptor protein 3 (NLRP3) and related genes have been determined in myelodysplastic syndrome (MDS), acute myeloid leukemia (AML), acute lymphocytic leukemia (ALL) and chronic myeloid leukemia (CML), revealing that certain polymorphisms in IL-1β, IL-18, nuclear factor-κB (NF-κB) or NLRP3 could be potential predictors of these malignant diseases [70,71,72,73]
This important role of the NLRP3 inflammasome in the pathogenesis of myeloid malignancies and the newly identified KRAS/RAC1/reactive oxygen species (ROS)/NLRP3/IL-1β axis has been demonstrated in chronic myelomonocytic leukemia (CMML), juvenile myelomonocytic leukemia (JNNL) and AML
The NLRP3 inflammasome has become a highly interesting topic in the last several years, and a growing number of studies have focused on the role of NLRP3 in hematopoietic malignancies
Summary
Chronic inflammation drives many types of cancers by promoting mutagenesis, preventing tumor surveillance, supporting clonal evolution and facilitating tumor spreading, among other effects [9,10] Both the avoidance of immune destruction and tumorpromoting inflammation were defined, among others, as hallmarks of cancer by Hanahan and Weinberg [11]. It is well-known that inflammation in the tumor microenvironment is associated with the release of various growth factors and proinflammatory cytokines, such as interleukin-1 (IL-1), IL-4, IL-6, tumor necrosis factor-α (TNF-α), transforming growth factor-β (TGF-β) and IL-10, able to promote tumorigenesis [11,12,13]. This review discusses chronic inflammation and the NLRP3 inflammasome in the context of leukemia and its preforms and briefly summarizes the current knowledge about their interrelationships
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