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      Targeting Gas6/TAM in cancer cells and tumor microenvironment

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          Abstract

          Growth arrest-specific 6, also known as Gas6, is a human gene encoding the Gas6 protein, which was originally found to be upregulated in growth-arrested fibroblasts. Gas6 is a member of the vitamin K-dependent family of proteins expressed in many human tissues and regulates several biological processes in cells, including proliferation, survival and migration, by binding to its receptors Tyro3, Axl and Mer (TAM). In recent years, the roles of Gas6/TAM signalling in cancer cells and the tumour microenvironment have been studied, and some progress has made in targeted therapy, providing new potential directions for future investigations of cancer treatment. In this review, we introduce the Gas6 and TAM receptors and describe their involvement in different cancers and discuss the roles of Gas6 in cancer cells, the tumour microenvironment and metastasis. Finally, we introduce recent studies on Gas6/TAM targeting in cancer therapy, which will assist in the experimental design of future analyses and increase the potential use of Gas6 as a therapeutic target for cancer.

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          Epithelial-mesenchymal transitions in development and disease.

          Jean Paul Thiery, Hervé Acloque, Ruby Y J Huang … (2009)
          The epithelial to mesenchymal transition (EMT) plays crucial roles in the formation of the body plan and in the differentiation of multiple tissues and organs. EMT also contributes to tissue repair, but it can adversely cause organ fibrosis and promote carcinoma progression through a variety of mechanisms. EMT endows cells with migratory and invasive properties, induces stem cell properties, prevents apoptosis and senescence, and contributes to immunosuppression. Thus, the mesenchymal state is associated with the capacity of cells to migrate to distant organs and maintain stemness, allowing their subsequent differentiation into multiple cell types during development and the initiation of metastasis.
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            Distinct role of macrophages in different tumor microenvironments.

            Claire Lewis, Jeffrey W Pollard (2006)
            Macrophages are prominent in the stromal compartment of virtually all types of malignancy. These highly versatile cells respond to the presence of stimuli in different parts of tumors with the release of a distinct repertoire of growth factors, cytokines, chemokines, and enzymes that regulate tumor growth, angiogenesis, invasion, and/or metastasis. The distinct microenvironments where tumor-associated macrophages (TAM) act include areas of invasion where TAMs promote cancer cell motility, stromal and perivascular areas where TAMs promote metastasis, and avascular and perinecrotic areas where hypoxic TAMs stimulate angiogenesis. This review will discuss the evidence for differential regulation of TAMs in these microenvironments and provide an overview of current attempts to target or use TAMs for therapeutic purposes.
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              Colony-stimulating factors in inflammation and autoimmunity.

              John Hamilton (2008)
              Although they were originally defined as haematopoietic-cell growth factors, colony-stimulating factors (CSFs) have been shown to have additional functions by acting directly on mature myeloid cells. Recent data from animal models indicate that the depletion of CSFs has therapeutic benefit in many inflammatory and/or autoimmune conditions and as a result, early-phase clinical trials targeting granulocyte/macrophage colony-stimulating factor and macrophage colony-stimulating factor have now commenced. The distinct biological features of CSFs offer opportunities for specific targeting, but with some associated risks. Here, I describe these biological features, discuss the probable specific outcomes of targeting CSFs in vivo and highlight outstanding questions that need to be addressed.
              Article 0 comments Cited 410 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Yang Yang:
                ORCID: http://orcid.org/0000-0002-1163-2359
                +86 13379217366 , yang200214yy@163.com
                Journal
                Journal ID (nlm-ta): Mol Cancer
                Journal ID (iso-abbrev): Mol. Cancer
                Title: Molecular Cancer
                Publisher: BioMed Central (London )
                ISSN (Electronic): 1476-4598
                Publication date (Electronic): 31 January 2018
                Publication date PMC-release: 31 January 2018
                Publication date Collection: 2018
                Volume: 17
                Electronic Location Identifier: 20
                Affiliations
                [1 ]ISNI 0000 0004 1761 5538, GRID grid.412262.1, Key Laboratory of Resource Biology and Biotechnology in Western China, Ministry of Education. Faculty of Life Sciences, , Northwest University, ; 229 Taibai North Road, Xi’an, 710069 China
                [2 ]ISNI 0000 0004 1761 4404, GRID grid.233520.5, Department of Aerospace Medicine, , The Fourth Military Medical University, ; 169 Changle West Road, Xi’an, 710032 China
                [3 ]ISNI 0000 0004 1791 6584, GRID grid.460007.5, Department of Thoracic Surgery, , Tangdu Hospital, The Fourth Military Medical University, ; 1 Xinsi Road, Xi’an, 710038 China
                [4 ]ISNI 0000 0004 1765 1045, GRID grid.410745.3, Department of Stomatology, , Bayi Hospital Affiliated to Nanjing University of Chinese Medicine, ; Nanjing, Jiangsu 210002 China
                [5 ]ISNI 0000 0004 1761 4404, GRID grid.233520.5, Department of Biomedical Engineering, , The Fourth Military Medical University, ; 169 Changle West Road, Xi’an, 710032 China
                [6 ]GRID grid.452438.c, Department of Cardiovascular Surgery, , The First Affiliated Hospital of Xi’an Jiaotong University, ; 277 Yanta West Road, Xi’an, Shaanxi 710061 China
                Author information
                http://orcid.org/0000-0002-1163-2359
                Article
                Publisher ID: 769
                DOI: 10.1186/s12943-018-0769-1
                PMC ID: 5793417
                PubMed ID: 29386018
                SO-VID: 5c1564c8-0a54-42a5-b1d5-133ecde0fbe5
                Copyright © © The Author(s). 2018
                License:

                Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                Date received : 26 July 2017
                Date accepted : 17 January 2018
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/501100001809, National Natural Science Foundation of China;
                Award ID: 81500263
                Award Recipient :
                Funded by: National Natural Science Foundation of China
                Award ID: 81600306
                Award Recipient :
                Funded by: FundRef http://dx.doi.org/10.13039/501100002858, China Postdoctoral Science Foundation;
                Award ID: 2016T90973
                Award Recipient :
                Funded by: China Postdoctoral Science Foundation
                Award ID: 2015M572681
                Award Recipient :
                Categories
                Subject: Review
                Custom metadata
                issue-copyright-statement © The Author(s) 2018

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: growth arrest-specific 6,cancer cells,tumour microenvironment
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: growth arrest-specific 6, cancer cells, tumour microenvironment

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