Table 1.
Tumor-derived exosomal ncRNAs promote macrophage polarization
| Exosomal ncRNAs | Cancer type | Expression levels in tumor cells and their exosomes | Potential direct target gene(s) of ncRNAs in macrophages | Mechanism | Macrophage polarization | Effect | Ref. | |
|---|---|---|---|---|---|---|---|---|
| miRNAs | miR-9 | HPV+ HNSCC | high | PPARδ↓ | downregulate PPARδ mRNA | M1 | increase the radiosensitivity of HPV+ HNSCC | Tong et al.46 |
| miR-451/miR-21 | GBM | high | c-Myc↓ | downregulate c-Myc mRNA | M2 | / | Van der Vos et al.47 | |
| miRNA let-7a-5p miRNAs let7-b, -g, -i | PCa | high | integrin-β3↓ | downregulate integrin-β3 | M2 | tumor migration | Ferguson et al.48 | |
| miR-21-5p | CRC | high | / | bind to TLR7 | M1 | liver metastasis | Shao et al.51 | |
| miR-125b-5p | melanoma | high in exosomes | LIPA↓ | target LIPA | M2 | / | Gerloff et al.52 | |
| miR-21 | bladder cancer | high | PTEN↓ | inhibit PTEN activation and increase STAT3 expression | M2 | cancer migration and invasion | Lin et al.56 | |
| miR-25-3p miR-130b-3p miR-425-5p |
CRC | high | PTEN↓ | downregulate PTEN and activate PI3K/AKT signaling | M2 | tumor metastasis by enhancing EMT and secreting VEGF | Wang and co-workers57,58 | |
| miR-29a-3p | oral squamous cell carcinoma | high | SOCS1↓ | regulate SOCS1/STAT6 signaling activity | M2 | cancer proliferation and invasion | Cai et al.62 | |
| miR-223 | CSCC | high | / | / | M1 | tumor progression | Zhang et al.63 | |
| miR-301a-3p | PC | high under hypoxic conditions | PTEN↓ | activate the PTEN/PI3Kγ signaling pathway | M2 | cancer migration, invasion, and EMT | Wang and co-workers66,67 | |
| miRNA let-7a | / | low in tumor cells and high in exosomes under hypoxic conditions | IRS-1, IRS-2, INSR, and IGF1R↓ | enhance oxidative phosphorylation and inhibit the insulin-Akt-mTOR signaling pathway | M2 | / | Park et al.69 | |
| miR-1246 | glioma | high under hypoxic conditions | TERF2IP↓ | target TERF2IP to activate STAT3 signaling and inhibit NF-κB signaling | M2 | cancer proliferation, migration, and invasion | Qian et al.70 | |
| miR-222-3p | EOC | high | SOCS3↓ | regulate the SOCS3/STAT3 pathway | M2 | cancer proliferation, migration | Ying et al.71 | |
| miR-940 | EOC | high under hypoxic conditions | / | / | M2 | tumor progression | Chen et al.72 | |
| miR-21-3p miR-125b-5p miR-181d-5p |
EOC | high under hypoxic conditions | SOCS4/5↓ | regulate the SOCS4/5/STAT3 pathway | M2 | cancer proliferation and migration | Chen et al.73 | |
| miR21 | head and neck cancer | high | PDCD4 and IL12A↓ | downregulate PDCD4 and IL12A | M2 | tumor growth and angiogenesis | Hsieh et al.78 | |
| miR-16 | BC | high after epigallocatechin gallate treatment | IKKα↓ | downregulate IKKα and accumulate Iκ-B to suppress NF-κB activity | M2→M1 | / | Jang et al.83 | |
| lncRNAs | lncRNA TUC339 | HCC | high | / | regulate cytokine receptor signaling pathways and CXCR chemokine receptor binding pathways | M2 | cancer proliferation and reduce cancer cell adhesion to the extracellular matrix | Kogure and co-workers49,50 |
| lncRNA DLX6-AS1 | HCC | high | miR-15a-5p↓ | regulate the miRNA-15a-5p/CXCL17 axis | M2 | cancer migration, invasion and EMT, including pulmonary metastasis | Wang et al.77 | |
| lncRNA RPPH1 | CRC | high | / | / | M2 | cancer metastasis and proliferation | Liang and co-workers79,80 | |
| lncRNA FGD5-AS1 | NSCLC | high | / | / | M2 | cancer migration and invasion | Lv et al.82 | |
| circRNAs | circFARSA | NSCLC | high | PTEN↓ | increase ubiquitination and degradation of PTEN and activate the PI3K/AKT signaling pathway | M2 | EMT and metastasis | Chen et al.59 |
| circ0048117 | ESCC | high under hypoxic conditions | miR-140↓ | act as a sponge of miR-140 by competing with TLR4 | M2 | tumor invasion and migration | Lu et al.68 | |
| circ0074854 | HCC | high | / | / | M2 | tumor migration and invasion | Wang et al.81 | |
| cicHIPK3 cicPTK2 |
NSCLC | high | / | / | M2 | Kras-associated chemoresistance | Katopodi et al.84 | |