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. 2021 Mar 27;12(2):15–37. doi: 10.4331/wjbc.v12.i2.15

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©The Author(s) 2021. Published by Baishideng Publishing Group Inc. All rights reserved.

This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/Licenses/by-nc/4.0/

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Modulation of angiogenesis by innate immune cells and other communicators in breast tumor microenvironment. In breast tumor microenvironment, innate immune cells and other communicators modulate angiogenesis. Tumor-associated macrophages promote angiogenesis by increasing the expression of CCL18, CD34, and microvascular density and assisting breast cancer cell modeling into stem cells for recruitment of immune-suppressive cells. Cancer-associated fibroblasts promote tumor angiogenesis by enhancing the expression of interleukin (IL) 6, IL-8, IL-11 and IL-15 as well as by changing the balance between pro-and anti-angiogenic factors via hypoxia-induced angiogenesis regulator. Tumor-derived exosomal Annexin II induce angiogenesis by recruiting macrophages to secrete IL-6 and tumor necrosis factor-α by activating p38MAPK, nuclear factor-κappa beta, and STAT3 signaling pathways. Exosomal miRNAs contribute to the development of tumor angiogenesis by enhancing the vasculature remodeling genes, Ephrin A3 and PTP1B. TAM: Tumor-associated macrophage; CAF: Cancer-associated fibroblast; HAIR: Hypoxia-induced angiogenesis regulator; NF-κβ: Nuclear factor-κappa beta; TNF: Tumor necrosis factor; IL: Interleukin; BC: Breast cancer.