Table 1.
Means of communication, transmitted factors, and the exerted effects between macrophages and different lung malignant cell types.
| Type of cell | Cancer | Direction of communication | Means of communication | Transmitted factors | Effects—molecular | Effects—biological | References |
|---|---|---|---|---|---|---|---|
| M2 | LUAD (H1395 and H197) | Macrophage—lung cancer cells | Conditioned media was added (exosomes or free secreted factors) | N/A | CXCL17 | Stimulation of spine metastasis | (72) |
| M2 | NSCLC | Lung cancer cells—Macrophage | N/A | N/A | p38 (p-p38) which further increases HIF-1α | Hypoxia induces M2 polarization through p38 | (73) |
| M2 | Lewis lung carcinoma | Macrophage—lung cancer cells | Chemokine receptors CCR2 and CX3CR1 chemokine receptor | IL-1, MIP1α0, IL-6, CCL1, G-CSF upregulated in the system | CCR2 and CX3CR1 upregulation after IL-10 or MIP1α exposure, upregulation of MMPs, GF, VEGF | Aggressiveness of lung cancer cell increased more in direct contact with macrophage than in non-contact culture | (68) |
| M2 | SCLC | Macrophage—lung cancer cells | Non-contact cell culture, culture media, soluble factors | IL-6 | STAT3 activation | Lung cancer cell proliferation and invasion | (69) |
| TAMs | NSCLC | Macrophage—lung cancer cells | Contact in vivo tumor | TNF-α | Depletion of TAMs resulted in decreased GLUT1, PDK1, PDH, PGK, HK2, G6P, VEGFA, CA-9, NOS2; PD-L1 | Increased glycolysis in cancer cells, decreased infiltrated T cells | (71) |
| M1/M2 | Lewis lung carcinoma | Macrophage (M2)—lung cancer cells | Non-contact cell culture, culture media, soluble factors | pAMK | Upregulation of AMPKα in the M2 macrophage | Migration/invasion | (74) |
| SIRPα expressing macrophage | SCLC | Lung cancer cells—Macrophage | Direct contact through antigen (CD47—tumor) and receptor (SIRPα–macrophage) | N/A | M2-like phenotype, without capacity of phagocytosis | (56) | |
| M2 | NSCLC | Macrophage—lung cancer cells | Secreted cytokines in the culture media (IL-10) | IL-10 | SOX2, Oct4, c-Myc, Vimentin, N-CAD - upregulation, phosphorylation of JAK1, STAT1/STAT3/STAT6, NOTCH1 | Cancer stemness and EMT | (58) |
| M2 | NSCLC | Macrophage—lung cancer cells | Secreted cytokines in the culture media IL-6 | IL-6 | E-CAD downregulation, VIM upregulation, β-catenin translocation in the nucleus, COX2, PGE2 upregulation | EMT | (70) |
| M2 | NSCLC | Lung cancer cells—Macrophage | Supernatant from cancer cells | IL-34 | Binding to the CSF-1R receptor, IL-10, and TGF-β overexpression | Polarization to anti-inflammatory phenotype, forms a feedback loop with cancer cells to sustain chemoresistance | (60) |
| M1 | Murine lung carcinoma cell lines (LLC26 and CMT 167) | Lung cancer cells—Macrophage | N/A | N/A | N/A | The lack of Caveolin-2 enhances local polarization of M1 macrophage, which further stimulates the local acquisition of CD8+ and CD4+ T cells, leading to smaller tumors | (67) |