Fig. 2

Direct interaction between TANs and tumor cells. Interactions between tumor cells and TANs typically lead to two outcomes: promotion or suppression, with the former involving necrosis or growth. The former one can be induced by type I IFN, IFN-γ and TNF-α, while the latter one by TGF-β [41, 85]. Necrosis of tumor cells can be induced not only by Antibody-dependent cell-mediated cytotoxicity (ADCC) of TANs through the combination of Fc receptors (FcR) and monoclonal antibodies (mAbs), but also by DNA damage and mutations triggered by ROS and reactive nitrogen species (RNS) [82, 83, 88]. The latter pathway may exhibit a paradoxical effect of promoting tumor growth and migration [82, 83]. Moreover, TANs secrete various molecules that can stimulate tumor growth, such as neutrophil elastase (NE), prostaglandin E2 (PGE2), TGF-β, and TGF-α [79,80,81]. Notably, mesenchymal cells expressing CD140a also produce PGE2, which contributes to the accumulation of lipid-rich TANs and subsequently fuels tumor growth through lipid oxidation [89]