Table 1 Role of NLRP3 inflammasome activation or suppression in cancer development
Type of cancer | Source of experimental evidence | Outcome | Suggested mechanism | References |
|---|---|---|---|---|
HNSCC | - HNSCC cell lines (A253) -Oral cancer tissue | Activation of NLRP3 inflmmasome closely associated with survival and invasiveness of HNSCC | Activation of IL-1β | [99] |
-HNSCC tissue - HNSCC cell lines(CAL27, SCC9, SCC25, and FaDu) - transgenic mouse HNSCC model | NLRP3 inflammasome related with the tumorgenesis and CSCs markers self-renewal activation | -overexpression of CSCs markers (BMI1, ALDH1 and CD44) | [100] | |
GBM | -U87 and GL261 xenograft mouse GBM model | NLRP3 inflammasome involved in resistance to radiotherapy | -regulation of numerous aging-related genes in hippocampus | [150] |
OSCC | - OSC cells lines (WS UHN6 and C AL27) -NLRP3−/− and Caspase1−/− mice -OSCC tissue | NLRP3 inflammasome increased resistance of OSCC to 5-FU | Promotion of the IL-1β production | [106] |
BC | - BC cell lines(LLC and E0771) -C57BL/6 mice | tumor-infiltrating regulation of NLRP3 strongly linked with tumor invasiveness, migration and outcome | IL-1β secretion and S1PR1 signaling | [123] |
GC | -GC tissue -GC cell lines (SGC-7901, BGC-823, HGC-27 and AGS) -normal gastric epithelial cell line (GES-1) | NLRP3 inflammasome stimulates epithelial cells proliferation and GC carcinogenesis | -IL-1 β secretion -enhance cyclin-D1 transcription | [77] |
CAC | -NLRP3−/−, Pycard−/− and Caspase1−/− mice | Mice with inflammasome compartment deficiency were extremely susceptible to AOM/DSS- induced colitis | -reduction in IL-18 | [67] |
-NLRP3−/− mouse | NLRP3−/− mouse is more susceptible to acute and recurrence CAC | -increasing pro–IL-1β and IL-18 secretion | [85] | |
-NLRP3−/− and Caspase1−/− mice | NLRP3−/− and Caspase1−/− mice were more susceptible to AOM/DSS-induced inflammation and increased tumor burdens | - NLRP3 inflammasome deficiency lead to reduction in secretion and activation of the tumor IFN-γ and STAT1 | [86] | |
-NLRP3−/−, ASC−/−, Caspase1−/−, cathepsin B−/− or cathepsin L−/−mice- | NLRP deficient mice were significantly protected from colitis | IL-1β secretion was abrogated in macrophages without NLRP3, ASC or Caspase-1 | [165] | |
CRC | -CRC and adjacent normal tissue | NLRP3 gene variation are correlated with worse survival | -elevatating IL-1β and IL-6 levels | [89] |
CRC metastatic in liver | -Inflammasome components −/− mouse | NLRP3 inflammasome inhibits liver CRC metastatic growth | -enhancing NK cell tumoricidal action | [91] |
Fibrosarcoma | -NLRP3−/− mouse model | NLRP3-deficient mice were less resistant to tumor formation | -NLRP3 suppressed NK cell | [116] |
Melanoma | -Human melanoma cell lines (A375) -mouse melanoma cell lines (B16F10) | Inhibition of NLRP3 inflmmasome blocked melanoma migration | -inhibition of NLRP3 inflmmasome suppressed secretion of cytokines IL-1β and IL-18 | [139] |
Cervical Cancer | -HPV+ and adjacent normal tissue | NLRP3 polymorphism related with a lower risk of HPV infection | -innate immune anti-viral response - obliteration of virus persistence and viral elimination | [144] |
Lung cancer | -human alveolar epithelial adenocarcinoma cell line (A549) | NLRP3 inflmmasome regulate the proliferation and metastasis of lung cancer | -promoting phosphorylation of Akt, ERK1/2, and CREB -enhancing the expression of Snail -decrement of E-cadherin expression | [112] |
HCC | -HCC tissues and adjacent normal tissues | -Down regulation of all of the NLRP3 inflammasome elements associated with HCC occurrence, advanced tumor stages and poor differentiation | NR | [96] |