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      Bipolar Tumor-Associated Macrophages in Ovarian Cancer as Targets for Therapy

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          Abstract

          Ovarian cancer, a rare but fatal disease, has been a challenging area in the field of gynecological cancer. Ovarian cancer is characterized by peritoneal metastasis, which is facilitated by a cross-talk between tumor cells and other cells in the tumor microenvironment (TME). In epithelial ovarian cancer, tumor-associated macrophages (TAMs) constitute over 50% of cells in the peritoneal TME and malignant ascites, and are potential targets for therapy. Here, we review the bipolar nature of TAMs and the evolving strategies to target TAMs in ovarian cancer.

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          IRF5 promotes inflammatory macrophage polarization and TH1-TH17 responses.

          Thomas Krausgruber, Katrina Blazek, Tim Smallie … (2011)
          Polymorphisms in the gene encoding the transcription factor IRF5 that lead to higher mRNA expression are associated with many autoimmune diseases. Here we show that IRF5 expression in macrophages was reversibly induced by inflammatory stimuli and contributed to the plasticity of macrophage polarization. High expression of IRF5 was characteristic of M1 macrophages, in which it directly activated transcription of the genes encoding interleukin 12 subunit p40 (IL-12p40), IL-12p35 and IL-23p19 and repressed the gene encoding IL-10. Consequently, those macrophages set up the environment for a potent T helper type 1 (T(H)1)-T(H)17 response. Global gene expression analysis demonstrated that exogenous IRF5 upregulated or downregulated expression of established phenotypic markers of M1 or M2 macrophages, respectively. Our data suggest a critical role for IRF5 in M1 macrophage polarization and define a previously unknown function for IRF5 as a transcriptional repressor.
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            CSF-1 receptor signaling in myeloid cells.

            E Richard Stanley, Violeta Chitu (2014)
            The CSF-1 receptor (CSF-1R) is activated by the homodimeric growth factors colony-stimulating factor-1 (CSF-1) and interleukin-34 (IL-34). It plays important roles in development and in innate immunity by regulating the development of most tissue macrophages and osteoclasts, of Langerhans cells of the skin, of Paneth cells of the small intestine, and of brain microglia. It also regulates the differentiation of neural progenitor cells and controls functions of oocytes and trophoblastic cells in the female reproductive tract. Owing to this broad tissue expression pattern, it plays a central role in neoplastic, inflammatory, and neurological diseases. In this review we summarize the evolution, structure, and regulation of expression of the CSF-1R gene. We discuss the structures of CSF-1, IL-34, and the CSF-1R and the mechanism of ligand binding to and activation of the receptor. We further describe the pathways regulating macrophage survival, proliferation, differentiation, and chemotaxis downstream from the CSF-1R. Copyright © 2014 Cold Spring Harbor Laboratory Press; all rights reserved.
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              Tissue macrophages: heterogeneity and functions

              Siamon Gordon, Annette Plüddemann (2017)
              Macrophages are present in all vertebrate tissues, from mid-gestation throughout life, constituting a widely dispersed organ system. They promote homeostasis by responding to internal and external changes within the body, not only as phagocytes in defence against microbes and in clearance of dead and senescent cells, but also through trophic, regulatory and repair functions. In this review, we describe macrophage phenotypic heterogeneity in different tissue environments, drawing particular attention to organ-specific functions. Electronic supplementary material The online version of this article (doi:10.1186/s12915-017-0392-4) contains supplementary material, which is available to authorized users.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Cancers (Basel)
                Journal ID (iso-abbrev): Cancers (Basel)
                Journal ID (publisher-id): cancers
                Title: Cancers
                Publisher: MDPI
                ISSN (Electronic): 2072-6694
                Publication date (Electronic): 29 September 2018
                Publication date Collection: October 2018
                Volume: 10
                Issue: 10
                Electronic Location Identifier: 366
                Affiliations
                [1 ]Division of Gynecologic Oncology, Department of Obstetrics and Gynecology, University of Kansas Medical Center, Kansas City, KS 66160, USA; vgupta@ 123456kumc.edu
                [2 ]Department of Pharmacology, Vanderbilt University, Nashville, TN 37232, USA; fiona.yull@ 123456vanderbilt.edu
                [3 ]Vanderbilt-Ingram Cancer Center, Nashville, TN 37232, USA
                [4 ]The University of Kansas Cancer Center, Kansas City, KS 66160, USA
                Author notes
                [* ]Correspondence: dkhabele@ 123456kumc.edu ; Tel.: +1-913-588-6225
                Author information
                https://orcid.org/0000-0003-1636-7942
                Article
                Publisher ID: cancers-10-00366
                DOI: 10.3390/cancers10100366
                PMC ID: 6210537
                PubMed ID: 30274280
                SO-VID: 1cdb4348-bfc9-4357-a2c0-2a27377526be
                Copyright © © 2018 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 22 August 2018
                Date accepted : 23 September 2018
                Categories
                Subject: Review

                Keywords: ovarian cancer,tumor-associated macrophages,peritoneal metastasis,tumor microenvironment
                Data availability:
                Keywords: ovarian cancer, tumor-associated macrophages, peritoneal metastasis, tumor microenvironment

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