Crosstalk of pyroptosis and cytokine in the tumor microenvironment: from mechanisms to clinical implication

Table 1 Role of participated cytokines in diverse programmed cell death

Type	Related cytokine(s)	Direct effect	Role in TME	Peripheral reaction	Reference
Pyroptosis	IL-1β, IL-18	Inflammasome formation	Amplify inflammation, activate immune response	Inflammatory reaction	[51]
Apotosis	TNF-α, Fas	Caspase activation	Maintain cellular homeostasis, suppress inflammation	No inflammatory response	[52, 53]
Autophagy	HIF‑1α	p27-E2F1 signaling pathway	Tumor angiogenesis, enhanced tumor growth	No inflammatory response	[54, 55]
Necroptosis	TNF-α, Fas, IFN-γ	RIPK3 activation, MLKL phosphorylation	Trigger inflammation	Inflammatory reaction	[56, 57]
Ferroptosis	TNF, IL-6, IL-1β	GPX4 regulation, TAM polarization	Induce inflammation-related immunosuppression	Inflammatory reaction	[58,59,60]
Cuproptosis	NA	NA	Promotion of tumor immune escape	Inflammatory reaction	[61]
Disulfidptosis	HMGB1	ICD hallmarks up-regulation	Antitumor immune response	Inflammatory reaction	[62]

Abbreviations: NA Not appliable, IL Interleukin, TNF Tumor necrosis factor, HIF‑1α Hypoxia-inducible factor 1 α, IFN Interferon, Fas Fas receptor (CD95), HMGB1 High mobility group box 1, RIPK3 Receptor-interacting serine/threonine-protein kinase 3, MLKL Mixed lineage kinase domain-like pseudokinase, GPX4 Glutathione peroxidase 4, TAM Tumor-associated macrophage, ICD Immunogenic cell death

ISSN: 1476-4598