Immunity, inflammation and cancer: a leading role for adenosine
Open accessAbstract
Cancer is a complex disease that is dictated by both cancer cell-intrinsic and cell-extrinsic processes. Adenosine is an ancient extracellular signalling molecule that can regulate almost all aspects of tissue function. As such, several studies have recently highlighted a crucial role for adenosine signalling in regulating the various aspects of cell-intrinsic and cell-extrinsic processes of cancer development. This Review critically discusses the role of adenosine and its receptors in regulating the complex interplay among immune, inflammatory, endothelial and cancer cells during the course of neoplastic disease.
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Adenosine accumulates in tumors during hypoxic stress and contributes to tumor progression via immune suppression and a direct effect on cancer cells.
“Adenosine accumulates in tumors during hypoxic stress and contributes to tumor progression via immune suppression and a direct effect on cancer cells.”
From Therapeutic targeting of hypoxia and hypoxia-inducible factors in cancer (2016) · cites this paper as Antonioli et al., 2013
Adenosine is a crucial factor mediating the hypoxic inhibition of the anti-tumor immune response.
“Adenosine is thus a crucial factor mediating the hypoxic inhibition of the anti-tumor immune response (Antonioli et al., 2013).”
From Therapeutic targeting of hypoxia and hypoxia-inducible factors in cancer (2016) · cites this paper as Antonioli et al., 2013
Overexpression of CD39 and CD73 lowers extracellular ATP and increases adenosine, abolishing immunogenicity of cell death.
“Moreover, overexpression of the ATP-degrading ectoenzymes ectonucleoside triphosphate diphosphohydrolase 1 (ENTPD1; best known as CD39) and 5′ nucleotidase, ecto (NT5E; best known as CD73) efficiently lowers extracellular ATP levels in favor of adenosine accumulation, hence abolishing the immunogenicity of cell death [902].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [902]
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References 218 · Cited by 765
- Authors
- Antonioli, L., Blandizzi, C., Pacher, P., & Haskó, G.
- Affiliations
- University of Pisa (IT)
- National Institutes of Health (US)
- University of Debrecen (HU)
- Corresponding author
- Haskó, György
- Venue
- Nature Reviews Cancer
- Published
- 2013-11-14
- Volume
- 13
- Issue
- 12
- Pages
- 842-857
- ISSN
- 1474-175X (ISSN-L)
- 1474-1768
- OpenAlex
- W2159945718
- Cited by
- 765
- References
- 218
- Citations by year
- 2026: 43 · 2025: 55 · 2024: 38 · 2023: 67 · 2022: 74 · 2021: 78 · 2020: 77 · 2019: 80 · 2018: 83 · 2017: 60 · 2016: 46 · 2015: 28 · 2014: 34 · 2013: 1
- FWCI
- 4.24
- Type
- journal article
- Language
- en
- Open access
- green
- www.nature.com
- Licence
- other-oa
- www.springer.com/tdm (tdm)
- Locations
- Nature reviews. Cancer (publishedVersion)
- PubMed (publishedVersion)
- CINECA IRIS Institutial research information system (University of Pisa) (submittedVersion)
- University of Debrecen Electronic Archive (University of Debrecen) (submittedVersion, other-oa)
- Funders
- National Institutes of Health
- National Institute of General Medical Sciences (R01 GM66189, R01GM066189)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Adenosine and Purinergic Signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Biochemical and Molecular Research
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Keywords
- adenosine, adenosine receptors, tumor immunology, inflammation, endothelial cells, tumor microenvironment, cancer
- MeSH terms
- Adenosine, Animals, Humans, Inflammation, Neoplasm Metastasis, Neoplasms, Receptors, Purinergic P1, Inflammation Mediators, Mitogen-Activated Protein Kinases, MAP Kinase Signaling System, Cell Proliferation, Tumor Microenvironment
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