MINI REVIEW article
Front. Immunol.
Sec. Molecular Innate Immunity
Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1677363
This article is part of the Research TopicMulti-Omics Interrogation of Tumor-Associated Macrophages: Paving the Way for Next-Generation Cancer ImmunotherapiesView all 4 articles
Roles of Tumor-Associated Macrophages in Triple-Negative Breast Cancer Progression
Provisionally accepted- The First Clinical College, Guangdong Medical University, Zhanjiang,524000, Guangdong, China., Zhanjiang, China
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Triple-negative breast cancer (TNBC) is an aggressive subtype characterized by the absence of estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2) expression. It is associated with a high risk of recurrence, metastasis, and limited therapeutic options. Tumor-associated macrophages (TAMs) play a central role in TNBC progression by shaping an immunosuppressive tumor microenvironment. Primarily polarized toward an M2-like phenotype under the influence of cytokines such as IL-10 and TGF-β, TAMs facilitate tumor growth, angiogenesis, metastasis, and immune evasion through multiple mechanisms. This review summarizes current understanding of TAM recruitment, polarization, and pro-tumoral functions in TNBC, and outlines emerging therapeutic strategies aimed at depleting TAMs, reprogramming them to an anti-tumor M1-like state, or blocking the CD47-SIRPα phagocytosis checkpoint. These approaches offer promising avenues for reprogramming the TNBC microenvironment and improving clinical outcomes.
Keywords: Triple-negative breast cancer, Tumor-associated macrophages, Tumor Microenvironment, Immune Evasion, TAM
Received: 31 Jul 2025; Accepted: 26 Sep 2025.
Copyright: © 2025 Wu and Liao. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Yuling Liao, w13078264@163.com
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