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      The adenosinergic system in cancer : Key therapeutic target

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      Author(s): , , *
      Publication date PMC-release:
      Journal: Oncoimmunology
      Publisher: Landes Bioscience
      Keywords: adenosine, adenosine receptors, ATP, CD73, tumor immunity

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          Abstract

          High amounts of adenosine are released in the tumor mass. Depending on the levels of adenosine, as well as on the receptor subtypes that are expressed by immune cells, adenosine can affect tumor growth in different fashions. Specifically targeting CD73, the rate-limiting enzyme for the extracellular generation of adenosine, or the A3 receptor offers new therapeutic strategies to limit tumor progression.

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          Extracellular adenosine triphosphate and adenosine in cancer.

          A Stagg, Joshua Smyth (2010)
          Adenosine triphosphate (ATP) is actively released in the extracellular environment in response to tissue damage and cellular stress. Through the activation of P2X and P2Y receptors, extracellular ATP enhances tissue repair, promotes the recruitment of immune phagocytes and dendritic cells, and acts as a co-activator of NLR family, pyrin domain-containing 3 (NLRP3) inflammasomes. The conversion of extracellular ATP to adenosine, in contrast, essentially through the enzymatic activity of the ecto-nucleotidases CD39 and CD73, acts as a negative-feedback mechanism to prevent excessive immune responses. Here we review the effects of extracellular ATP and adenosine on tumorigenesis. First, we summarize the functions of extracellular ATP and adenosine in the context of tumor immunity. Second, we present an overview of the immunosuppressive and pro-angiogenic effects of extracellular adenosine. Third, we present experimental evidence that extracellular ATP and adenosine receptors are expressed by tumor cells and enhance tumor growth. Finally, we discuss recent studies, including our own work, which suggest that therapeutic approaches that promote ATP-mediated activation of inflammasomes, or inhibit the accumulation of tumor-derived extracellular adenosine, may constitute effective new means to induce anticancer activity.
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            Tumor cell death and ATP release prime dendritic cells and efficient anticancer immunity.

            Antoine Tesniere, Deborah J Smyth, Lionel Apetoh … (2010)
            By destroying tumor cells, conventional anticancer therapies may stimulate the host immune system to eliminate residual disease. Anthracyclines, oxaliplatin, and ionizing irradiation activate a type of tumor cell death that elicits efficient anticancer immune responses depending on interferon gamma (IFNgamma) and the IFNgamma receptor. Thus, dying tumor cells emit danger signals that are perceived by dendritic cells (DC), which link innate and cognate immune responses. Recently, we observed that ATP was released by tumor cells succumbing to chemotherapy. ATP activates purinergic P2RX7 receptors on DC, thus activating the NLRP3/ASC/caspase-1 inflammasome and driving the secretion of interleukin-1beta (IL-1beta). IL-1beta then is required for the adequate polarization of IFNgamma-producing CD8(+) T cells. These results imply a novel danger signal, ATP, and a novel receptor, P2RX7, in the chemotherapy-elicited anticancer immune response.
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              CD73: a novel target for cancer immunotherapy.

              Bin Zhang (2010)
              The promise of cancer immunotherapy has not been translated into clinical successes, in large part because of tumor-associated immune suppression that blocks effective antitumor immunity. Recent findings show a tumor-induced immunosuppressive mechanism, whereby tumor-derived CD73 functions as an ecto-enzyme to produce extracellular adenosine, which promotes tumor growth by limiting antitumor T-cell immunity via adenosine receptor signaling. Results with small molecule inhibitors, or monoclonal antibodies targeting CD73 in murine tumor models, suggest that targeted CD73 therapy is an important alternative and realistic approach to effective control of tumor growth. In particular, it helps T-cell-based therapy by enhancing the adaptive immune response machinery, which may increase the function of tumor-infiltrating T lymphocytes, and subsequently lead to improved survival in cancer patients. (c)2010 AACR.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Oncoimmunology
                Journal ID (iso-abbrev): Oncoimmunology
                Journal ID (publisher-id): ONCI
                Title: Oncoimmunology
                Publisher: Landes Bioscience
                ISSN (Print): 2162-4011
                ISSN (Electronic): 2162-402X
                Publication date (Print): 01 January 2013
                Publication date PMC-release: 01 January 2013
                Volume: 2
                Issue: 1
                Electronic Location Identifier: e22448
                Affiliations
                Department of Pharmaceutical and Biomedical Sciences; University of Salerno; Salerno, Italy
                Author notes
                [* ]Correspondence to: Silvana Morello, Email: smorello@ 123456unisa.it
                Article
                Publisher ID: 2012ONCOIMM0313 Publisher Item ID: 22448
                DOI: 10.4161/onci.22448
                PMC ID: 3583919
                PubMed ID: 23483072
                SO-VID: 32ea4088-8845-4654-935c-3cbdff4dbf1e
                Copyright © Copyright © 2013 Landes Bioscience
                License:

                This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.

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                ScienceOpen disciplines: Immunology
                Keywords: adenosine,adenosine receptors,atp,cd73,tumor immunity
                Data availability:
                ScienceOpen disciplines: Immunology
                Keywords: adenosine, adenosine receptors, atp, cd73, tumor immunity

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