Table 2.

Tumor-derived factors inducing NETosis.

Factor/Tumor-Associated Condition	Source	Possible Mechanisms of Action	References
Amyloid β	CAFs [166]	Directs the formation of tumor-associated NETs via CD11b and ROS-dependent mechanism	[166]
Cathepsin C	Tumor cells [174]	Induces neutrophil recruitment and NET production via the PR3-IL-1β-NF-κB axis	[174]
Complement component C3a	C3 proteolysis in the extracellular environment, tumor cells [193]	Causes neutrophils recruitment to the tumor microenvironment as well as LDN recruitment to liver metastasis sites	[193,194]
CXCL5	CAFs [163] and tumor cells [195]	Enhances neutrophil chemotaxis via the ERK/p38 pathway	[196,197]
CXCL6/ huGCP-2	Tumor cells [164]	Chemoattractant for neutrophils; NETosis induction via CXCR2	[198]
EVs	CAFs [199] and tumor cells [200]	Chemoattractant for neutrophils; depending on the load, they can change the phenotype of neutrophils; trigger NETosis, NF-κB pathway activation	[145,200]
G-CSF	CAFs and tumor cells [166]	NETosis induction via NOX, MPO, and ROS	[200,201]
Hypoxia		Regulation of NET release via the mTOR pathway and increased HIF-1α expression	[157]
Il-8	Tumor cells [156], endothelial cells [202]	Chemoattractant for neutrophils; induction of NETosis through CXCR2, followed by activation of the PI3K/p38/NF-kB pathway; possible induction via NOX, MPO, and ROS	[165,203,204,205]
IL-17	Th17, CD4+, and γδ T cells [206]	Mediates recruitment of neutrophils via CD8+ T cells, IL-17-Th (mechanism unknown)	[206]