Inflammatory cells in tumor angiogenesis, metastasis, and antiangiogenic drug response (IMAGE)
Caption
. Tumor-associated macrophages (TAMs) and tumor-associated neutrophils (TANs) produce various proangiogenic growth factors and cytokines such as vascular endothelial growth factor (VEGF), tumor necrosis factor-alpha (TNF-a), and interleukin-6 (IL-6) to stimulate angiogenesis. Neovascularization facilitates recruitment of TAMs and TANs in tumors. b. Inflammatory cells in cancer metastasis. TAMs in primary tumors facilitate tumor cell dissemination and invasion by formation of TAM-tumor cell clusters, which facilitate intravasation of tumor cells through the vessel wall. Within the circulation, TAMs may aid tumor cells to the distal organ, where they facilitate tumor cell extravasation. TAMs probably prepare metastatic niches and trigger angiogenesis in the metastatic organs to ensure the regrowth of metastases. c. TAMs, TANs, and other myeloid cells significantly contribute to antiangiogenic drug (AAD) resistance. In response to AADs, tumors experience high levels of hypoxia due to pruning of microvessels. Hypoxia induced production of manifold non-VEGF angiogenic factors that are not AAD targets. Through this mechanism, tumors deploy non-VEGF factors to induce neovascularization and develop AAD resistance. EC = endothelial cell; VEGFR2 = vascular endothelial growth factor 2; PC = pericyte; IL-33 = interleukin-33; PECAM-1 = platelet endothelial cell adhesion molecule; BV8 = bombina variegata; FGF = fibroblast growth factor; G-CSF = granulocyte-colony stimulating factor; CXCL = C-X-C motif ligand.
Credit
Prof. Yihai Cao from Karolinska Institute, Sweden Image source link: https://link.springer.com/article/10.1007/s44466-025-00021-1
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