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Pathways Regulating Macrophage Phagocytosis of Tumor Cells

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: closed (15 December 2023) | Viewed by 4639

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Guest Editor
Department of Biological Sciences, School of Integrative Science and Technology, Kean University, Union, NJ 07083, USA
Interests: cancer; glioblastoma; invasion; macrophages; microenvironment; microglia; chemokines; metastasis
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Special Issue Information

Dear Colleagues,

Cancer immunotherapy has yielded exciting results in the clinic. Thus far the majority of approaches has been focused on stimulating the cytotoxic T lymphocyte (CTL) response to cancer cells by either targeting immune checkpoints (PD-L1 and CTLA4) or by genetic manipulation of the patient’s T cells with chimeric antigen receptors (CAR-T). However, recruiting macrophages in the fight against cancer has been gaining more attention recently. In particular, antibody-mediated blockade of the CD47 “don’t eat me” receptor to stimulate phagocytosis of tumor cells has been experimentally validated in animal models and is currently undergoing clinical trials. In addition, genetic engineering and modification of patient monocyte/macrophages ex-vivo using CAR-M therapy is an emerging approach which holds great promise as an effective strategy for attacking solid tumors. The regulation and mechanism of macrophage phagocytosis of cancer cells however is complex and likely involves many cell-surface receptors and signaling pathways. This special edition focuses on the juxtacrine interactions between tumor associated macrophages and cancer cells which can promote phagocytosis and potentially be harnessed for therapeutic application.

Dr. Salvatore Coniglio
Guest Editor

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Published Papers (1 paper)

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Review

14 pages, 2213 KiB  
Review
Impact of Lipid Metabolism on Macrophage Polarization: Implications for Inflammation and Tumor Immunity
by Evros Vassiliou and Renalison Farias-Pereira
Int. J. Mol. Sci. 2023, 24(15), 12032; https://doi.org/10.3390/ijms241512032 - 27 Jul 2023
Cited by 9 | Viewed by 4268
Abstract
Macrophage polarization is influenced by lipids, which also exert significant control over macrophage functions. Lipids and their metabolites are players in intricate signaling pathways that modulate macrophages’ responses to pathogens, phagocytosis, ferroptosis, and inflammation. This review focuses on lipid metabolism and macrophage functions [...] Read more.
Macrophage polarization is influenced by lipids, which also exert significant control over macrophage functions. Lipids and their metabolites are players in intricate signaling pathways that modulate macrophages’ responses to pathogens, phagocytosis, ferroptosis, and inflammation. This review focuses on lipid metabolism and macrophage functions and addresses potential molecular targets for the treatment of macrophage-related diseases. While lipogenesis is crucial for lipid accumulation and phagocytosis in M1 macrophages, M2 macrophages likely rely on fatty acid β-oxidation to utilize fatty acids as their primary energy source. Cholesterol metabolism, regulated by factors such as SREBPs, PPARs, and LXRs, is associated with the cholesterol efflux capacity and the formation of foam cells (M2-like macrophages). Foam cells, which are targets for atherosclerosis, are associated with an increase in inflammatory cytokines. Lipolysis and fatty acid uptake markers, such as CD36, also contribute to the production of cytokines. Enhancing the immune system through the inhibition of lipid-metabolism-related factors can potentially serve as a targeted approach against tumor cells. Cyclooxygenase inhibitors, which block the conversion of arachidonic acid into various inflammatory mediators, influence macrophage polarization and have generated attention in cancer research. Full article
(This article belongs to the Special Issue Pathways Regulating Macrophage Phagocytosis of Tumor Cells)
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