Table 2.

Tumor-derived molecules acting in tumor-associated macrophage (TAM) formation in cervical cancer (CC).

Categories	Name of Molecules	Potential Mechanism
Molecules promoting the differentiation of monocytes to TAMs	PGE2 and IL-6 [28]
	Karyopherin β1	Regulating the expression of transcriptional factors NFκB and AP-1 [29]
	CCL2 /MCP-1	Promoting the recruitment of circulating monocytes [30] Enhancing the LPS-induced production of IL-10 [30]
	IL-10	Inhibit the classic activation of macrophages through the JAK1/Tyk2/STAT3 pathway [31]
	PRL	Inducing IL-1β and TNF-α production [32] Inducing the production of anti-inflammatory cytokine IL-10 [33]
Molecules promoting the activation of TAMs	FUCA-1	Affecting the activity of LPS receptor on macrophages [34] Affecting the cytotoxicity of macrophages to tumor cells [34]
	GM-CSF	Promoting TAMs to release pro-tumor factors [35]
	MIF [36]
	IL-10	Elevating the expression of IL-4Rα [37] Elevating arginase 1 [37]

The table shows tumor-derived molecules and their potential mechanism to form TAMs. PGE2, prostaglandin E2; IL-6, interleukin 6; MCP-1, monocyte chemoattractant protein 1, its alternative name is CCL2; IL-10, interleukin 10; PRL, prolactin; FUCA-1, α-l-Fucosidase; GM-CSF, granulocyte macrophage colony-stimulating factor; MIF, Macrophage migration inhibitory factor; LPS, lipopolysaccharide; TNF-α, tumor necrosis factor α; IL-4R, interleukin 4 receptor.