TABLE 1.
The regulation mechanisms of phenotypic polarisation of tumour‐associated macrophages (TAMs) in gastric cancer (GC).
| Objects | Expression | Sources | Mechanisms | Outcome | References |
|---|---|---|---|---|---|
| EGFR transactivation | – | Macrophages | IL‐4‐stimulated HB‐EGF‐dependent transactivation of EGFR inhibited the polarisation of M2 TAMs induced by IL‐4‐stimulated STAT6 activation. | EGFR transactivation promoted M1 TAMs polarisation | 14 |
| STING pathway | High expression in GC tissues (200 paired) and macrophages | Macrophages | Knocking‐down STING activated the IL‐6R–JAK–STAT pathway | Knocking‐down STING promoted M1 TAMs polarisation | 32 |
| DOK1 | Low expression in GC tissues (64) and high expression in M1 TAMs (56) | Macrophages | DOK1 activated the NF‐κB pathway | DOK1 promoted M1 TAMs polarisation | 33 |
| CDK5RAP3 | Low expression in GC tissues (241) with high M2 TAMs content | GC cells | CDK5RAP3 inhibited the IL‐4 and IL‐10 by repressing the NF‐κB pathway | CDK5RAP3 promoted M1 TAMs polarisation | 39 |
| CXCL5 | High expression in GC tissues (103) with high M2 TAMs content | Macrophages | – | CXCL5 promoted M2 TAMs polarisation | 41 |
| CXCL8 | High expression in GC tissues (8 paired) | Macrophages | CXCL8 enhanced the secretions of IL‐10 by activating the JAK–STAT1 pathway of GC cells | CXCL8 promoted M2 TAMs polarisation | 42 |
| YAP1 | High expression in GC tissues (32 paired) | GC cells | YAP1 enhanced the secretions of IL‐3 in GC cells | YAP1 promoted M2 TAMs polarisation | 43 |
| Lipids | – | GC cells | Lipid accumulation activated the PI3K‐γ pathway | Lipids promoted M2 TAMs polarisation | 44 |
| USP14 | High expression in GC tissues (20 paired) | Macrophages | USP14 enhanced the fatty acid oxidation by stabilising SIRT1/PGC1‐α axis | USP14 promoted M2 TAMs polarisation | 45 |
| MSR1 | High expression in GC tissues (21 paired) | Macrophages | MSR1 activated the AMPK/mTOR pathway | MSR1 promoted M2 TAMs polarisation | 46 |
| MAT2A | High expression in CD14+ cells from tumour tissues compared with that from peripheral blood of GC patients (15) | Macrophages | MAT2A enhanced the RIP1 expression by increasing WDR5 | MAT2A promoted M2 TAMs polarisation | 47 |
| IGFBP7 | – | CAFs | IGFBP7 activated FGFR1/PI3K/AKT axis through increasing secretions of FGF2 | IGFBP7 promoted M2 TAMs polarisation | 48 |
| IL‐6/IL‐8 | – | MSCs | IL‐6 and IL‐8 activated the JAK2/STAT3 pathway | IL‐6 and IL‐8 promoted M2 TAMs polarisation | 51 , 61 |
| Exosomal miR‐519a‐3p | High expression in cells with high liver metastasis potential and in serum from GC patients with liver metastasis (75) | GC cells | Exosomal miR‐519a‐3p activated the MAPK/ERK pathway by targeting DUSP2 | Exosomal miR‐519a‐3p promoted M2 TAMs polarisation | 52 |
| ADAMTS10 | Low expression in GC tissues (64 paired) | GC cells | ADAMTS10 elevated ROS levels by increasing TXNIP expression through inhibiting JAK/STAT/c‐MYC pathway | ADAMTS10 promoted M1 TAMs polarisation | 59 |
| Dextran sulphate | – | – | Dextran sulphate blocked the IL‐6–STAT3 pathway induced by IL‐4 and IL‐13 | Dextran sulphate promoted M1 TAMs polarisation | 60 |
| Exosomal circ_0017252 | Low expression in GC tissues and serum (5 paired) | GC cells | – | Exosomal circ_0017252 promoted M1 TAMs polarisation | 64 |
| Exosomal lnc‐MIR4435‐2HG | – | GC cells | Exosomal lnc‐MIR4435‐2HG activated the Jagged1/Notch and JAK1/STAT3 axes | Exosomal lnc‐MIR4435‐2HG promoted M2 TAMs polarisation | 65 |
| Exosomal PKM2 | – | GC cells | Exosomal PKM2 increased the Egr‐1 | Exosomal PKM2 promoted M2 TAMs polarisation | 66 |
| Exosomal miR‐151‐3p | High expression in GC tissues (35) | GC cells | – | Exosomal miR‐151‐3p promoted M2 TAMs polarisation | 67 |
| Exosomal lnc‐HCG18 | High expression in GC tissues (28 paired) | GC cells | Exosomal lnc‐HCG18 increased the KLF4 by targeting miR‐875‐3p | Exosomal lnc‐HCG18 promoted M2 TAMs polarisation | 68 |
| Sophoridine | – | – | Sophoridine activated the TLR4/IRF3 axis | Sophoridine promoted M1 TAMs polarisation | 73 |
| PTX3 | Low expression in GC tissues (30 paired) | GC cells | PTX3 reduced the secretions of IL‐4 and IL‐10 from GC cells by inhibiting phosphorylation of the JNK1/2 | PTX3 promoted M1 TAMs polarisation | 77 |
| DKK1 | High expression in GC tissues (284 tumour samples and 32 paired normal tissues) | GC cells | DKK1 interacted with CKAP4 on the macrophage surface and activated downstream PI3K–AKT signalling | DKK1 promoted M2 TAMs polarisation | 81 |
| POU1F1 | High expression in GC tissues (60 paired) | GC cells | HMGA1B/2 triggered CXCL12/CXCR4 axis by transcriptionally activating POU1F1 | POU1F1 promoted M2 TAMs polarisation | 83 |
| CRIP1 | High expression in GC tissues (81 paired) | GC cells | CRIP1 increased the CCL5 secretion by promoting phosphorylation of CREB1 | CRIP1 promoted M2 TAMs polarisation | 85 |
| LINC00665 | High expression in M2 TAMs | Macrophages | LINC00665 activated the Wnt1 by binding to BACH1 | LINC00665 promoted M2 TAMs polarisation | 87 |
| LncRNA ANCR | High expression in GC tissues (60) | Macrophages | LncRNA ANCR inhibited the expression of FoxO1 | LncRNA ANCR promoted M2 TAMs polarisation | 88 |
| CALM2 | High expression in GC tissues (31 paired) and cell lines | GC cells | CALM2 increased the CXCL12, IL‐4, IL‐13 and IL‐10 by activating JAK2/STAT3/HIF‐1 signalling | CALM2 promoted M2 TAMs polarisation | 90 |
| ELK4 | High expression in GC tissues (30 paired) and GC‐TAMs | Macrophages | ELK4 increased the KSR1 by regulating the KDM5A–PJA2 axis | ELK4 promoted M2 TAMs polarisation | 92 |
| Lactic acid | – | GC cells | Lactic acid triggered MCT–HIF1α signalling | Lactic acid promoted M2 TAMs polarisation | 108 |
Abbreviations: AMPK/mTOR, AMP‐activated protein kinase/mammalian target of rapamycin; CAFs, cancer‐associated fibroblasts; CCL, C‐C motif chemokine ligand; HB‐EGF, heparin binding‐epidermal growth factor; IL, interleukin; MCT–HIF1α, monocarboxylate channel transporter‐hypoxia inducible factor 1 subunit alpha; MSCs, mesenchymal stromal cells; NF‐κB, nuclear factor‐kappa B; PI3K/Akt, phosphatidylinositol‐3‐kinase/protein kinase B; ROS, reactive oxygen species.