TREM-1low is a novel characteristic for tumor-associated macrophages in lung cancer

Zhang, Guangbo; Li, Hongmei; Huang, Jian; Chen, Siwen; Pan, Xudong; Huang, Haitao

doi:10.18632/oncotarget.9639

Cited by 8 publications

(6 citation statements)

References 22 publications

(40 reference statements)

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“…Further research is crucial before immunotherapeutic strategies based on TREM-1 targeting could be translated into clinical settings. Divergent results were in fact reported by Zhang et al [244], who showed that TREM-1 expression in TAMs and Mn were decreased during lung tumor progression. An additional level of complexity is given by the evidence of TREM-1 expression on other myeloid and non-myeloid cells involved in anti-tumor responses [37].…”

Section: Discussionmentioning

confidence: 83%

Targeting Mononuclear Phagocyte Receptors in Cancer Immunotherapy: New Perspectives of the Triggering Receptor Expressed on Myeloid Cells (TREM-1)

Raggi

Bosco

2020

Cancers

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Inflammatory cells are major players in the onset of cancer. The degree of inflammation and type of inflammatory cells in the tumor microenvironment (TME) are responsible for tilting the balance between tumor progression and regression. Cancer-related inflammation has also been shown to influence the efficacy of conventional therapy. Mononuclear phagocytes (MPs) represent a major component of the inflammatory circuit that promotes tumor progression. Despite their potential to activate immunosurveillance and exert anti-tumor responses, MPs are subverted by the tumor to support its growth, immune evasion, and spread. MP responses in the TME are dictated by a network of stimuli integrated through the cross-talk between activatory and inhibitory receptors. Alterations in receptor expression/signaling can create excessive inflammation and, when chronic, promote tumorigenesis. Research advances have led to the development of new therapeutic strategies aimed at receptor targeting to induce a tumor-infiltrating MP switch from a cancer-supportive toward an anti-tumor phenotype, demonstrating efficacy in different human cancers. This review provides an overview of the role of MP receptors in inflammation-mediated carcinogenesis and discusses the most recent updates regarding their targeting for immunotherapeutic purposes. We focus in particular on the TREM-1 receptor, a major amplifier of MP inflammatory responses, highlighting its relevance in the development and progression of several types of inflammation-associated malignancies and the promises of its inhibition for cancer immunotherapy.

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Section: Discussionmentioning

confidence: 83%

Targeting Mononuclear Phagocyte Receptors in Cancer Immunotherapy: New Perspectives of the Triggering Receptor Expressed on Myeloid Cells (TREM-1)

Raggi

Bosco

2020

Cancers

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“…Similarly, TREM-1 expression on neutrophils was comparable in neutrophils isolated from healthy colonic tissue of untreated control mice, AOM/DSS-induced tumors, as well as adjacent tumor-free, colonic tissues of treated mice (data not shown). Interestingly, a recent study has even reported progressive loss of TREM-1 on tumor-infiltrating monocytes/macrophages in a mouse lung carcinoma model and proposed TREM-1 low expression as a novel characteristic for TAMs in human NSCLC tissue 52 . Thus, the expression and functional significance of TREM-1 on cells of the monocyte/macrophage lineage seems to depend on the tissue-dependent context or the nature of tumor-associated inflammation and calls for further investigation across distinct types of cancer.…”

Section: Discussionmentioning

confidence: 99%

TREM-1 promotes intestinal tumorigenesis

Saurer

Zysset

Rihs

et al. 2017

Sci Rep

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Triggering receptor expressed on myeloid cells-1 (TREM-1) is a potent amplifier of pro-inflammatory innate immune responses. Increasing evidence suggests a role for TREM-1 not only in acute pathogen-induced reactions but also in chronic and non-infectious inflammatory disorders, including various types of cancer. Here, we demonstrate that genetic deficiency in Trem1 protects from colorectal cancer. In particular, Trem1 −/− mice exhibited reduced tumor numbers and load in an experimental model of inflammation-driven tumorigenesis. Gene expression analysis of Trem1 −/− versus Trem1 +/+ tumor tissue demonstrated distinct immune signatures. Whereas Trem1 −/− tumors showed an increased abundance of transcripts linked to adaptive immunity, Trem1 +/+ tumors were characterized by overexpression of innate pro-inflammatory genes associated with tumorigenesis. Compared to adjacent tumor-free colonic mucosa, expression of Trem1 was increased in murine and human colorectal tumors. Unexpectedly, TREM-1 was not detected on tumor-associated Ly6C− MHC class II+ macrophages. In contrast, TREM-1 was highly expressed by tumor-infiltrating neutrophils which represented the predominant myeloid population in Trem1 +/+ but not in Trem1 −/− tumors. Collectively, our findings demonstrate a clear role of TREM-1 for intestinal tumorigenesis and indicate TREM-1-expressing neutrophils as critical players in colorectal tumor development.

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“…The expression of TREM-1 on TAMs decreases significantly with tumor growth, which is a feature of lung cancer TAMs. In addition, TREM-1 activation can promote TAM to secrete IL-1b in the intervention of LPS (195). This also indicates that the low expression level of TREM-1 in TAMs may affect the pro-inflammatory effect of TAMs, which is beneficial to tumor growth.…”

Section: Target Other Signaling Moleculesmentioning

confidence: 96%

The Crosstalk Between Tumor-Associated Macrophages (TAMs) and Tumor Cells and the Corresponding Targeted Therapy

2020

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Tumor microenvironment (TME) is composed of tumor cells and surrounding non-tumor stromal cells, mainly including tumor associated macrophages (TAMs), endothelial cells, and carcinoma-associated fibroblasts (CAFs). The TAMs are the major components of non-tumor stromal cells, and play an important role in promoting the occurrence and development of tumors. Macrophages originate from bone marrow hematopoietic stem cells and embryonic yolk sacs. There is close crosstalk between TAMs and tumor cells. With the occurrence of tumors, tumor cells secrete various chemokines to recruit monocytes to infiltrate tumor tissues and further promote their M2-type polarization. Importantly, M2-like TAMs can in turn accelerate tumor growth, promote tumor cell invasion and metastasis, and inhibit immune killing to promote tumor progression. Therefore, targeting TAMs in tumor tissues has become one of the principal strategies in current tumor immunotherapy. Current treatment strategies focus on reducing macrophage infiltration in tumor tissues and reprogramming TAMs to M1like to kill tumors. Although these treatments have had some success, their effects are still limited. This paper mainly summarized the recruitment and polarization of macrophages by tumors, the support of TAMs for the growth of tumors, and the research progress of TAMs targeting tumors, to provide new treatment strategies for tumor immunotherapy.

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TREM-1low is a novel characteristic for tumor-associated macrophages in lung cancer

Cited by 8 publications

References 22 publications

Targeting Mononuclear Phagocyte Receptors in Cancer Immunotherapy: New Perspectives of the Triggering Receptor Expressed on Myeloid Cells (TREM-1)

Targeting Mononuclear Phagocyte Receptors in Cancer Immunotherapy: New Perspectives of the Triggering Receptor Expressed on Myeloid Cells (TREM-1)

TREM-1 promotes intestinal tumorigenesis

The Crosstalk Between Tumor-Associated Macrophages (TAMs) and Tumor Cells and the Corresponding Targeted Therapy

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