Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2017 Mar 14;8(11):18486-18496.
doi: 10.18632/oncotarget.14474.

Targeting macrophage anti-tumor activity to suppress melanoma progression

Huafeng Wang  1 , Lijuan Zhang  1   2 , Luhong Yang  1 , Chengfang Liu  3 , Qi Zhang  4 , Linjing Zhang  1
Affiliations
Review

Targeting macrophage anti-tumor activity to suppress melanoma progression

Huafeng Wang et al. Oncotarget. .

Abstract

By phagocytosing cancer cells and their cellular debris, macrophages play a critical role in nonspecific defense (innate immunity) and, as antigen presenters, they help initiate specific defense mechanisms (adaptive immunity). Malignant melanoma is a lethal disease due to its aggressive capacity for metastasis and resistance to therapy. For decades, considerable effort has gone into development of an effective immunotherapy for treatment of metastatic melanoma. In this review, we focus on the anti-tumor activities of macrophages in melanoma and their potential as therapeutic targets in melanoma. Although macrophages can be re-educated through intercellular signaling to promote tumor survival owing to their plasticity, we expect that targeting the anti-tumor activity of macrophages remains a promising strategy for melanoma inhibition. The combination of tumoricidal macrophage activation and other treatments such as surgery, chemotherapy, and radiotherapy, may provide an effective and comprehensive anti-melanoma strategy.

Keywords: GM-CSF; immunoadjuvant agent; macrophage; melanoma.

PubMed Disclaimer

Conflict of interest statement

CONFLICTS OF INTEREST

The authors declare that there is no conflict of interest.

Figures

Figure 1
Figure 1. Xenogeneic activation of macrophages strategies
These macrophages were cultured in vitro with various supernatants obtained from xenogeneic lymphocytes after their interaction with the tumor in vitro
Figure 2
Figure 2. Immunoembolization with tumoricidal macrophage aggregation
Embolization agents combined with GM-CSF are infused by blood vessel to melanoma sites, which results in disruption of the tumor blood supply and the local immunologic reaction evoked by GM-CSF stimulating hepatic macrophages.
Figure 3
Figure 3. Tumoricidal macrophages are induced by Th1 cells
Th1 cells characteristically express IFN-γ, CD40 ligand, lymphotoxin-alpha (LT-α) by their receptors on macrophages to stimulate macrophages into the potent tumoricidal effector cells, which generate tumoricidal reactive oxygen and nitrogen species, and enhance fusion of phagosomes with lysosomes.
Figure 4
Figure 4. Biphasic effects of IFN-γ on melanoma
Application of IFN-γ to melanoma treatment (Left). Adverse effects of IFN-γ on melanoma by pro-expression of MHC-I or CD74 (Right).
Figure 5
Figure 5. Melanoma inhibits macrophages
Melanoma cell release programmed cell death-1 ligand 1 (PD-L1) and macrophage inhibitory cytokine-1 (MIC) that suppress the macrophage activation.
See this image and copyright information in PMC

References

    1. National Cancer Institute (USA)); Aug 25, 2015. Melanoma Treatment-for health professionals (PDQ®)
    1. Organization WH . WHO Report Geneva: WHO; 2014. 2014. World cancer report. Chapter 5.14.
    1. Siegel RL, Miller KD, Jemal A. Cancer statistics, 2015. CA Cancer J Clin. 2015;65(1):5–29. - PubMed
    1. committee; Cme China's guidelines of diagnosis and treatment of melanoma(2011) Chinese Clinical Oncology. 2012;02:159–171.
    1. Han Y, Qu X. The current situations and advances in cutaneous malignant melanoma. Modern Journal of Integrated Traditional Chinese and Western Medicine. 2015;30:3416–3420.

Substances