Abstract
Drug resistance is one of the most critical challenges in breast cancer (BC) treatment. The occurrence and development of drug resistance are closely related to the tumor immune microenvironment (TIME). Tumor-associated macrophages (TAMs), the most important immune cells in TIME, are essential for drug resistance in BC treatment. In this article, we summarize the effects of TAMs on the resistance of various drugs in endocrine therapy, chemotherapy, targeted therapy, and immunotherapy, and their underlying mechanisms. Based on the current overview of the key role of TAMs in drug resistance, we discuss the potential possibility for targeting TAMs to reduce drug resistance in BC treatment, By inhibiting the recruitment of TAMs, depleting the number of TAMs, regulating the polarization of TAMs and enhancing the phagocytosis of TAMs. Evidences in our review support it is important to develop novel therapeutic strategies to target TAMs in BC to overcome the treatment of resistance.
Highlights
Of all female cancers, breast cancer (BC) is the most common cancer with the highest morbidity and mortality in women [1]
Endocrine therapy (ET) is seen as the standard treatment for Luminal BC, chemotherapy is the preferred treatment for Triple-negative breast cancer (TNBC), targeted therapy is commonly used for HER2 positive BC treatment, and immunotherapy has been demonstrated to have the best therapeutic efficacy in TNBC, so it is most widely used in the treatment of TNBC
Tumor-associated macrophages (TAMs) promote the development of BC treatment resistance based on the unilateral effect of TAM on breast cancer cells (BCCs) but through a feedback loop interaction between TAMs and BCCs in many cases
Summary
BC is the most common cancer with the highest morbidity and mortality in women [1]. TAM and BC’s Drug Resistance the development of resistance to BC therapy is strongly linked to genetic mutations, metabolic reprogramming, breast cancer stem cells, EMT and hypoxia of the tumor microenvironment. These alterations are usually associated with the activation of a range of related signaling pathways, as well as the expression of associated signaling molecules (Figure 1). Various signaling pathways, including NF-kB, Hedgehog, and JAK/STAT activation, affect BC treatment resistance by influencing the metabolic reprogramming of BCCs, CSC and EMT [21,22,23,24,25,26]. This review will focus on the current status of the treatment of various subtypes of BC, the impact of TAMs on the resistance of each subtype of BC, and an overview of the solutions to the resistance of BC
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