Macrophages as a Double-Edged Weapon: The Use of Macrophages in Cancer Immunotherapy and Understanding the Cross-Talk Between Macrophages and Cancer

Salah, Ahmed; Li, Yanqin; Wang, Hao; Qi, Nianmin; Wu, Yuehong

doi:10.1089/dna.2020.6087

Cited by 9 publications

(7 citation statements)

References 126 publications

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“…In addition to impacting the GBM proliferation, our transwell migration data also revealed that MIF1 was able to induce cellular metastasis and invasion of GBM cells when cocultured with M1, M2 or MIF1-induced macrophages. Indeed, these observations clearly fit the model of double function of macrophages, whereby M1 macrophages are responsible for wound healing in the normal context, but those normal functions being responsible for tumor growth and malignancy, and M2 macrophages are responsible for immune responses [44].…”

Section: Discussionsupporting

confidence: 70%

Musashi-1 Regulates MIF1-Mediated M2 Macrophage Polarization in Promoting Glioblastoma Progression

Yang

Chien

Yarmishyn

et al. 2021

Cancers

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Glioblastoma (GBM) is the most malignant brain tumor which is characterized by high proliferation and migration capacity. The poor survival rate has been attributed to limitations of the current standard therapies. The search for novel biological targets that can effectively hamper tumor progression remains extremely challenging. Previous studies indicated that tumor-associated macrophages (TAMs) are the abundant elements in the tumor microenvironment that are closely implicated in glioma progression and tumor pathogenesis. M2 type TAMs are immunosuppressive and promote GBM proliferation. RNA-binding protein Musashi-1 (MSI1) has recently been identified as a marker of neural stem/progenitor cells, and its high expression has been shown to correlate with the growth of GBM. Nevertheless, the relationship between MSI1 and TAMs in GBM is still unknown. Thus, in our present study, we aimed to investigate the molecular interplay between MSI1 and TAMs in contributing to GBM tumorigenesis. Our data revealed that the secretion of macrophage inhibitory factor 1 (MIF1) is significantly upregulated by MSI1 overexpression in vitro. Importantly, M2 surface markers of THP-1-derived macrophages were induced by recombinant MIF1 and reduced by using MIF1 inhibitor (S,R)-3-(4-hHydroxyphenyl)-4,5-dihydro-5-isoxazole acetic acid (ISO-1). Furthermore, GBM tumor model data suggested that the tumor growth, MIF1 expression and M2 macrophage population were significantly downregulated when MSI1 expression was silenced in vivo. Collectively, our findings identified a novel role of MSI1 in the secretion of MIF1 and the consequent polarization of macrophages into the M2 phenotype in promoting GBM tumor progression.

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Section: Discussionsupporting

confidence: 70%

Musashi-1 Regulates MIF1-Mediated M2 Macrophage Polarization in Promoting Glioblastoma Progression

Yang

Chien

Yarmishyn

et al. 2021

Cancers

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“…Macrophages were mainly divided into M1 and M2 macrophages. M1 macrophages represented the proinflammatory subtype, activating the immune response, while M2 macrophages constructed an immunosuppressive microenvironment through anti-inflammatory activity [ 42 ]. M1 macrophages as drug carriers accounted for tumor inhibition in gliomas [ 43 ].…”

Section: Discussionmentioning

confidence: 99%

Development of a Hallmark Pathway-Related Gene Signature Associated with Immune Response for Lower Grade Gliomas

Lai

Zhong

Liu

et al. 2022

IJMS

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Although some biomarkers have been used to predict prognosis of lower-grade gliomas (LGGs), a pathway-related signature associated with immune response has not been developed. A key signaling pathway was determined according to the lowest adjusted p value among 50 hallmark pathways. The least absolute shrinkage and selection operator (LASSO) and stepwise multivariate Cox analyses were performed to construct a pathway-related gene signature. Somatic mutation, drug sensitivity and prediction of immunotherapy analyses were conducted to reveal the value of this signature in targeted therapies. In this study, an allograft rejection (AR) pathway was considered as a crucial signaling pathway, and we constructed an AR-related five-gene signature, which can independently predict the prognosis of LGGs. High-AR LGG patients had higher tumor mutation burden (TMB), Immunophenscore (IPS), IMmuno-PREdictive Score (IMPRES), T cell-inflamed gene expression profile (GEP) score and MHC I association immunoscore (MIAS) than low-AR patients. Most importantly, our signature can be validated in four immunotherapy cohorts. Furthermore, IC50 values of the six classic chemotherapeutic drugs were significantly elevated in the low-AR group compared with the high-AR group. This signature might be regarded as an underlying biomarker in predicting prognosis for LGGs, possibly providing more therapeutic strategies for future clinical research.

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“…Phenotypically and functionally similar to M2 macrophages are CD163 and CD206 expressing tumor-associated M2-like macrophages (M2 TAMs) [ 86 ]. TAMs originate from peripheral blood monocytes that infiltrate into the tumor microenvironment in response to cytokines such as VEGF, colony stimulating factor-1 (CSF1), CXC motif chemokine ligand-12 (CXCL12) and various CC motif chemokine ligands (CCL) such as CCL2 [ 87 , 88 ].…”

Section: The Role Of the Immunosuppressive Microenvironment In The Pr...mentioning

confidence: 99%

Treating Multiple Myeloma in the Context of the Bone Marrow Microenvironment

Xiao

et al. 2022

Current Oncology

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The treatment landscape of multiple myeloma (MM) has evolved considerably with the FDA-approval of at least 15 drugs over the past two decades. Together with the use of autologous stem cell transplantation, these novel therapies have resulted in significant survival benefit for patients with MM. In particular, our improved understanding of the BM and immune microenvironment has led to the development of highly effective immunotherapies that have demonstrated unprecedented response rates even in the multiple refractory disease setting. However, MM remains challenging to treat especially in a high-risk setting. A key mediator of therapeutic resistance in MM is the bone marrow (BM) microenvironment; a deeper understanding is necessary to facilitate the development of therapies that target MM in the context of the BM milieu to elicit deeper and more durable responses with the ultimate goal of long-term control or a cure of MM. In this review, we discuss our current understanding of the role the BM microenvironment plays in MM pathogenesis, with a focus on its immunosuppressive nature. We also review FDA-approved immunotherapies currently in clinical use and highlight promising immunotherapeutic approaches on the horizon.

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Macrophages as a Double-Edged Weapon: The Use of Macrophages in Cancer Immunotherapy and Understanding the Cross-Talk Between Macrophages and Cancer

Cited by 9 publications

References 126 publications

Musashi-1 Regulates MIF1-Mediated M2 Macrophage Polarization in Promoting Glioblastoma Progression

Musashi-1 Regulates MIF1-Mediated M2 Macrophage Polarization in Promoting Glioblastoma Progression

Development of a Hallmark Pathway-Related Gene Signature Associated with Immune Response for Lower Grade Gliomas

Treating Multiple Myeloma in the Context of the Bone Marrow Microenvironment

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