Table 2.

Effects of chemokines in the crosstalk between TAMs and tumor

Chemokines	Receptors	Cancer type	Function	Mechanism	References
CCL2	CCR2	Retinoblastoma	Recruitment of TAMs in the TME	The CCL2-CCR2 axis was activated	[26]
CCL2	CCR2	Pancreatic cancer	Formation of immunosuppressive TAMs	CCL2 recruited CCR2 + inflammatory monocytes to migrate to tumors	[27]
CCL2	CCR2	Esophageal squamous carcinoma	Blocked the recruitment of TAMs	Blocked the CCL2-CCR2 signaling pathway	[28]
CCL2	CCR2	Esophageal squamous carcinoma	Immune escape	M2 polarization increased the expression of PD-L2 in TAMs	[28]
CCL2	CCR2	Gastric cancer	Recruitment of TAMs in the TME	Increased CCL2 secretion	[29]
CCL2	CCR2	Hepatocellular carcinoma	Inflammatory monocyte recruitment and infiltration were reduced; the M2 polarization of TAMs was inhibited	CCL2 gene was knocked out or CCL2-CCR2 signaling pathway was blocked	[30]
CCL3	CCR5/CCR1	Pediatric high-grade glioma	TAMs infiltration is inhibited	Knocked out the CCL3 gene	[38]
CCL3	CCR5	Esophageal squamous cell carcinoma	Enhanced the ability of TAMs to promote the invasion and metastasis of tumor cells	The CCL3-CCR5 axis activated phosphorylation of Extracellular regulated protein kinases (ERK) and PAK	[39]
CCL3	CCR1	Gastric cancer	The recruitment of TAMs in TME increased and The M2-phenotype polarization of TAMs is promoted	CCL3-CCR1 interaction	[40]
CCL3	CCR5/CCR1	Intrahepatic cholangiocarcinoma	Adjusted the TME	M2 macrophages increased the secretion of cytokines (GM-CSF, TNF-α, Intercellular cell adhesion molecule-1 (ICAM-1), IL-6, etc.) and chemokines (CCL1, CCL3, etc.)	[41]
CCL5	CCR5	Malignant phyllodes tumor	The recruitment and repolarization of TAMs	CCL5-CCR5-driven signal cascade reaction	[47]
CCL5	CCR5	Liver cancer	M2 TAMs polarization	Through the CCL5-CCR5 signaling pathway	[48]
CCL5	CCR5	Gastric cancer	Promoted the proliferation, invasion and metastasis of tumors	TAMs secreted large amounts of CCL5	[49]
CCL5	CCR5	Prostate cancer	Promoted chemical resistance and distant metastasis of prostate cancer	TAMs-mediated STAT3-dependent epithelial–mesenchymal transformation by secreting CCL5	[50]
CCL5	CCR5	Gastric cancer	Promoted gastric cancer progression	TAMs-mediated GSN silencing by increasing the expression of DNMT1 in gastric cancer cells through the CCL5-CCR5、STAT3 signaling pathway	[51]
CCL5	CCR5	Breast cancer	Enhanced the ability of TAMs to promote tumor metastasis	Through the CCL5—CCR5 axis	[52]
CCL18	CCR8	Gallbladder carcinoma	Promoted tumor invasion and metastasis	M2 TAMs activated PI3K/Akt signaling by secreting CCL18	[57]
CCL18	CCR8	Ovarian cancer	EMT and metastasis	The M2 TAMs released CCL18	[58]
CCL18	CCR8	Colorectal cancer, Osteosarcoma, Head and neck squamous cell carcinoma, Breast cancer, Pancreatic ductal adenocarcinoma, lung cancer	Promoted tumor invasion and metastasis	M2 TAMs secreted CCL18	[59–67, 69]
CCL18	CCR8	Breast cancer	Promoted tumor angiogenesis	M2 TAMs secreted CCL18	[69]
CCL18	CCR8	Non-small cell lung cancer	Exerted immunosuppressive effect	CCL18+TAMs inhibited the production of inflammatory factors	[70]
CCL15	CCR1	Follicular thyroid carcinoma	Recruitment of TAMs in the TME	Tumors secreted CCL15	[77]
CCL15	CCR1	Squamous cell carcinoma of the head and neck	Developed resistance to gefitinib	Paracrined CCL15 of M2 TAMs and through the CCL15-CCR1-NF-κB pathway	[78]
CCL26	CX3CR1	Colorectal cancer	TAMs infiltration	PRL-3 raised CCL26	[83]
CXCL8	CXCR1/CXCR2	Cancer	Recruitment of TAMs in tumors	Circulating hypoxia activated HIF-1 and NF-κB in tumor cells, which led to increased production of VEGF-A, CCL2/ MCP-1, CXCL1/GRO-α, CXCL8/IL-8 and PGE2	[90]
CXCL8	CXCR1/CXCR2	Bladder cancer	Promoted tumor invasion and metastasis and immunosuppression	The invasion of TAMs in TME led to the elevation of CXCL8, which in turn promoted the secretion of MMP-9, VEGF and E-cadherin(E-Cad) by bladder cancer cells	[91]
CXCL8	CXCR1/CXCR2	Gastric carcinoma	immunosuppression	CSF-2 promoted TAMs secretion of CXCL8, which induced decreased infiltration of CD8 + T cells and increased PD-L1 expression on macrophages, thereby inhibiting CD8 + T cell activity	[92]
CXCL8	CXCR1/CXCR2	Breast cancer	Enhanced the migration, invasion and EMT ability	TAMs secreted CXCL8	[93]
CXCL8	CXCR1/CXCR2	Oral squamous cell carcinoma	Promoted the differentiation of monocyte-derived TAMs	The tumor secreted IL-8	[94]
CXCL8	CXCR1/CXCR2	Epithelial ovarian cancer	Interfered with the differentiation of monocyte-derived TAMs	Neutralizing monoclonal antibodies against IL-8 were used	[95]
CXCL12	CXCR4	Colorectal cancer	Induced TAM migration	sirtuin 1(SIRT1) passed through the CXCR4-CXCL12 pathway	[100]
CXCL12	CXCR4	Gastric carcinoma	Regulated the polarization of TAMs to M2 macrophages in tumor	pituitary transcription factor (POU Class 1 Homeobox 1, POU1F1) passed through the CXCL12-CXCR4 axis	[101]
CXCL12	CXCR4	Oral squamous cell carcinoma	Induced M2 macrophages polarization	cancer-associated fibroblasts (CAFs) passed through the CXCL12-CXCR4 signaling pathway	[102]
CXCL12	CXCR4	Ovarian cancer	Promoted M2 to M1 polarization of TAMs in tumors	The expression of CXCL12 and CXCR4 in tumor cells was downregulated	[103]
CXCL12	CXCR4	Prostate Cancer	Promoted the survival of cancer cells after chemotherapy	Increased secretion of CXCL12 by TAMs led to activation of its receptor CXCR4	[104]
CXCL12	CXCR4	Adenocarcinoma of the colon and stomach	Promoted TAMs-mediated CD8 + T cell inhibition	The activation of CXCL12-CXCR4	[105]
CXCL12	CXCR4	Cancer	Tumor cell infiltration	The unidirectional transition from migrating macrophages to perivascular macrophages is regulated by CXCL12 and CXCR4	[106]
CX3CL1	CX3CR1	Skin cancer, liver cancer	M2 TAMs were recruited	Through the CX3CL1-CX3CR1 axis	[21, 115]
CX3CL1	CX3CR1	Breast cancer, testicular reproductive carcinoma	The invasion of TAMs in the tumor	Increased CX3CL1 expression	[113, 114]
CX3CL1	CX3CR1	Cancer	TAMs infiltration was increased in TME and promoted angiogenesis	Activation of CX3CR1 inhibited TAMs apoptosis	[118]