Abstract
Deregulated inflammation is considered to be one of the hallmarks of cancer initiation and development regulation. Emerging evidence indicates that the inflammasome plays a central role in regulating immune cells and cytokines related to cancer. The inflammasome is a multimeric complex consisting of NOD-like receptors (NLRs) and responds to a variety of endogenous (damage-associated molecular patterns) and exogenous (pathogen-associated molecular patterns) stimuli. Several lines of evidence suggests that in cancer the inflammasome is positively associated with characteristics such as elevated levels of IL-1β and IL-18, activation of NF-κB signaling, enhanced mitochondrial oxidative stress, and activation of autophagic process. A number of NLRs, such as NLRP3 and NLRC4 are also highlighted in carcinogenesis and closely correlate to chemoresponse and prognosis. Although conflicting evidence suggested the duplex role of inflammasome in cancer development, the phenomenon might be attributed to NLRs difference, cell and tissue type, cancer stage, and specific experimental conditions. Given the promising role of inflammasome in mediating cancer development, precise elucidation of its signaling network and pathological significance may lead to novel therapeutic options for malignancy therapy and prevention.
Highlights
Inflammation is recognized as a major hallmark of cancer
On the other hand, during tumor progression and metastasis, cytokines or chemokines secreted by immune cells lead to an increase in cell survival, motility and invasiveness, such as epithelialmesenchymal transition (EMT) [10,11,12]
Gemcitabine and 5-fluorouracil exert increased antitumor effects when tumors were established in NLRP3-/- or Caspase-1-/mice, and NLRP3 activation by chemotherapeutic drugs is considered to be a positive regulator to promote cancer growth [101]. All these findings suggest the protumorigenic role of NLRP3 in cancer development
Summary
Inflammation is recognized as a major hallmark of cancer. As early as 1863, Rudolph Virchow speculated on a link between cancer and inflammation based on the observation of leukocyte infiltration in human breast cancer [1, 2]. Type I interferon is capable of suppressing caspase-1 activity by activation of the transcription factor, STAT1, subsequently inhibiting NLRP3 and NLRP1 inflammasome (Figure 3) [48].
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