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Review
. 2013 Feb;138(2):93-104.
doi: 10.1111/imm.12023.

Anti-tumour strategies aiming to target tumour-associated macrophages

Xiaoqiang Tang  1 , Chunfen Mo, Yongsheng Wang, Dandan Wei, Hengyi Xiao
Affiliations
Review

Anti-tumour strategies aiming to target tumour-associated macrophages

Xiaoqiang Tang et al. Immunology. 2013 Feb.

Abstract

Tumour-associated macrophages (TAMs) represent a predominant population of inflammatory cells that present in solid tumours. TAMs are mostly characterized as alternatively activated M2-like macrophages and are known to orchestrate nearly all stages of tumour progression. Experimental investigations indicate that TAMs contribute to drug-resistance and radio-protective effects, and clinical evidence shows that an elevated number of TAMs and their M2 profile are correlated with therapy failure and poor prognosis in cancer patients. Recently, many studies on TAM-targeted strategies have made significant progress and some pilot works have achieved encouraging results. Among these, connections between some anti-tumour drugs and their influence on TAMs have been suggested. In this review, we will summarize recent advances in TAM-targeted strategies for tumour therapy. Based on the proposed mechanisms, those strategies are grouped into four categories: (i) inhibiting macrophage recruitment; (ii) suppressing TAM survival; (iii) enhancing M1-like tumoricidal activity of TAMs; (iv) blocking M2-like tumour-promoting activity of TAMs. It is desired that further attention be drawn to this research field and more effort be made to promote TAM-targeted tumour therapy.

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Figures

Figure 1
Figure 1
Tumour-associated macrophage (TAM) -targeted anti-tumour strategy. Since the functions of TAMs depend on their accumulation and activation, present TAM-targeted approaches mainly concentrate on four aspects: (i) inhibiting macrophage recruitment; (ii) suppressing TAM survival; (iii) enhancing M1 tumoricidal activity; and (iv) blocking M2 tumour-promoting activity. CCL, C-C motif chemokine ligand; M-CSF, macrophage-colony-stimulating factor; CXCL12, C-X-C motif chemokine ligand 12; VEGF, vascular endothelial growth factor; HIF, hypoxia-inducible factor; FRβ, folate receptor β; NF-κB, nuclear factor κB; TLR, Toll-like receptor; STAT, signal transducers and activators of transcription; SHIP, Src homology 2-containing inositol-5'-phosphatase; GM-CSF, granulocyte–macrophage colony-stimulating factor; PPAR, peroxisome proliferator-activated receptor; PI3K, phosphatidylinositol 3-kinase; KLF4, Krüppel-like factor 4; Ets2, E26 transcription-specific sequence 2; DcR3, Decoy receptor 3; TSC2-mTOR, tuberous sclerosis complex 2-mammalian target of rapamycin; HRG, histidine-rich glycoprotein; MDXAA, 5,6-dimethylxanthenone-4-acetic acid; PPZ, proton pump inhibitor pantoprazole.
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