Table 1.

The contrasting roles of inflammasomes in cancer.

Tumour Types	Roles of Inflammasomes	Inflammasomes and Signalling Molecules		Results	Reference
NPC	Tumour suppressor	NLRP3, IL-1β		Upregulation tumour inflammasome-derived IL-1β actively induced the influx of TANs to the tumour site and positively correlated to patient survival.	[44]
	Tumour promoter	Caspase-1, IL-1β, IL-18		Constitutive activation of caspase-1 facilitated EBV genome persistence and immune evasion.	[103]
Multiple myeloma	Tumour promoter	NLRP1, IL-18		NLRP1-mediated IL-18 induced immunosuppression through MDSC recruitment.	[21]
OSCC	Tumour promoter	NLRP3		Knockdown of NLRP3 increased E-cadherin expression and suppressed proliferation, invasion, and migration of OSCC cells.	[136]
Melanoma	Tumour promoter	NLRP3, IL-1β		NLRP3 activation increased IL-1β secretion, resulting in auto-inflammation and enhanced tumour growth.	[137]
Breast cancer	Tumour promoter	NLRP1, IL-1β, IL-18	NLRP1 promoted tumour progression by inducing EMT, both in vivo and in vitro.		[138]
	Tumour promoter	NLRP3, IL-1β	NLRP3 activation and IL-1β promoted tumour growth and lung metastasis via increased infiltration of MDSCs and TAMs.		[139]
	Tumour suppressor	Caspase-1	Downregulation of caspase-1 increased breast cancer cell proliferation and invasion.		[140]
Lung cancer	Tumour promoter	NLRP3	NLRP3 activation decreased E-cadherin expression and promoted proliferation and migration of lung cancer cells.		[141]
	Tumour suppressor	NLRP3, Caspase-1	Impairment of NLRP3/caspase-1 activation promoted immunosuppression in the lung microenvironment.		[142]
CRC	Tumour promoter	NLRP3	Knockdown of NLRP3 reversed mesenchymal phenotypes of tumour cells and diminished tumour migration and invasion.		[143]
	Tumour suppressor	NLRP3, IL-18	NLRP3-derived IL-18 enhanced NK cell priming and trigger FasL-induced apoptosis of CRC cells.		[144]
	Tumour suppressor	NLRP3, IL-18	NLRP3 activation enhanced maturation and tumouricidal activity of NK cells as well as suppressed metastatic growth of CRC in liver.		[49,145]
HNSCC	Tumour promoter	NLRP3, IL-1β	Upregulation of NLRP3 activity positively correlated to carcinogenesis and CSC markers.		[146]
	-	NLRP3, P2X7R	Blockade of NLRP3 activation and P2X7R significantly reduced invasiveness and viability of HNSCC cells.		[147]
Pancreatic cancer	Tumour promoter	NLRP3, caspase-1, IL-1β	NLRP3 activation promoted tumour survival via upregulation of caspase-1 activity and IL-1β production.		[148]
	-	NLRP3, ASC, caspase-1	Inhibition of NLRP3, ASC, or caspase-1 activation restored innate and adaptive antitumour immune response.		[149]
CAC	Tumour suppressor	NLRP1, NLRP3, IL-1β, IL-18	Loss of inflammasome-secreted IL-1β and IL-18 increased susceptibility of mice to CAC.		[150,151]
	-	NLRP3, IL-18	Defective NLRP3 activation decreased IL-18 production and led to the overgrowth of commensal, massive infiltration of leucocytes, and overproduction of chemokines in the colon, which ultimately, resulted in increased mortality rates.		[152]

NPC, nasopharyngeal cancer; NLRP3, NOD-like receptor pyrin domain containing 3; IL-1β, interleukin-1β; TANs, tumour-associated neutrophils; IL-18, interleukin-18; EBV, Epstein–Barr virus; NLRP1, NOD-like receptor pyrin domain containing 1; MDSCs, myeloid-derived suppressor cells; OSCC, oral squamous cell carcinoma; EMT, epithelial-mesenchymal transition; TAMs, tumour-associated macrophages; CRC, colorectal cancer; NK cells, natural killer cells; HNSCC, head and neck squamous cell carcinoma; CSC, cancer stem cell; P2X7R, P2X7 purinergic receptor; ASC, apoptosis-associated speck-like protein; CAC, colitis-associated cancer.