Table 1.
Therapeutic TAM-modulating agents for osteosarcoma
Therapeutic agent | Targeted cell or molecule | Mechanism | Reference |
---|---|---|---|
Mifamurtide (MTP-PE) | Monocytes and macrophages | Switches TAM polarization toward an intermediate M1-M2 phenotype | 474 |
pSTAT3, pAKT, IL-17R TNF-a, IL-1, IL-6, IL-8, NO, PGE2, and PGD2 LFA-1, ICAM-1 and, HLA-DR |
Switches TAM polarization toward an intermediate M1-M2 phenotype | 475 | |
ATRA | CD117+ Stro-1+ cells, cancer stem cells, and macrophages | Decreases M2-like TAMs | 125 |
IL-1b, IL-4, IL-6, IL-13, and CXCL8 |
Decreases M2 phenotype polarization-mediated stemness | 476 | |
Esculetin |
LM8 cells and macrophages Cyclin D1, CDK 4, MMP-2, TGF-b1, VEGF, IL-10, MCP-1, and pSTAT3 |
Downregulates essential cytokines (TGFb1, IL-10, and MCP-1) and proteins (pSTAT3) Involved in the differentiation of M2 macrophages | 299 |
Zoledronic acid | Monocytes, DCs, and macrophages | Upregulates M1-like cytokines | 73 |
IL-1β, TNF-α, VEGF, IL-10, IDO, IL-12, and poly I:C TGF-β, Arg-1, and Fizz-1 |
Downregulates M2-like cytokines | 477 | |
Porous hollow iron nanoparticles |
Macrophages PI3K g and NF-kB p65 |
Upregulates NF-kB p65 and downregulates PI3K g in TAMs | 478 |
Chimeric antigen receptor macrophages |
T cells, dendritic cells, and macrophages ERK and NF-kB (P65) |
Upregulates pro-inflammatory pathways (interferon signaling, the TH1 pathway, and iNOS signaling) in M2 macrophages | 479 |