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Review
. 2022 Aug 26;24(4):640.
doi: 10.3892/etm.2022.11577. eCollection 2022 Oct.

Macrophages in melanoma: A double‑edged sword and targeted therapy strategies (Review)

Qiujun Zhou  1 , Tingting Fang  1 , Shenyu Wei  2 , Shiqian Chai  1 , Huifeng Yang  1 , Maocan Tao  3 , Yi Cao  3
Affiliations
Review

Macrophages in melanoma: A double‑edged sword and targeted therapy strategies (Review)

Qiujun Zhou et al. Exp Ther Med. .

Abstract

Melanoma, which evolves from melanocytes, is the most malignant skin cancer and is highly fatal, although it only accounts for 4% of all skin cancers. Numerous studies have demonstrated that melanoma has a large tumor mutational burden, which means that melanoma has great potential to achieve immune evasion. Tumor-associated macrophages (TAMs) are an important component of both the immune system and tumor microenvironment. Several studies have demonstrated their double-edged sword effects on melanoma. The present review focuses on the role of TAMs in melanoma development, including regulation of proliferation, invasion, metastasis, angiogenesis and chemical resistance of melanoma. Furthermore, the existing mechanisms of action of the TAM-targeting treatments for melanoma are reviewed. More broadly, the weak points of existing research and the direction of future research are finally identified and described.

Keywords: double-edged sword; macrophages; melanoma; targeted therapy.

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Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Figure 1
Figure 1
Classification of TAMs and their dual roles in tumors. TAM, tumor-associated macrophage; LPS, lipopolysaccharide; CCL17, C-C motif chemokine ligand 17.
Figure 2
Figure 2
Potential strategies for treating melanoma by targeting macrophages. (Left) Depleting TAMs by regulating CSF1R receptors, thereby interfering with tumor killing by CD8+ T cells. (Middle) Enhanced tumor killing by CD8+ T cells by reprogramming TAMs to promote M1-type polarization of macrophages. (Right) Regulation of tumor killing by CD8+ T cells by targeting functional molecules of TAMs. This figure has been adapted from Fig. 1C of the article ‘Targeting Tumor-Associated Macrophages as a Potential Strategy to Enhance the Response to Immune Checkpoint Inhibitors’ (100). Front. Cell Dev. Biol., 04 April 2018 | https://doi.org/10.3389/fcell.2018.00 © 2018 Cassetta and Kitamura. ARG1, arginase 1; CSF1R, colony-stimulating factor 1 receptor; FcγR, Fc-γ receptor; HDAC, histone deacetylase; MARCO, macrophage receptor with collagenous structure; PLX3397, pexidartinib; TAM, tumor-associated macrophage.
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Grants and funding

Funding: This study was funded by the Traditional Chinese Medicine Specialist Inheritance Studio (grant no. GZS2020022) and the Zhejiang Medical and Health Research Project (grant no. 2020KY447).