Abstract
Evaluation of: Beavis PA, Divisekera U, Paget C et al. Blockade of A2A receptors potently suppresses the metastasis of CD73(+) tumors. Proc. Natl Acad. Sci. USA 110(36), 14711-14716 (2013). CD73 is becoming an emerging therapeutic target for the prevention of tumor growth and metastasis. However, the mechanism by which CD73 promotes tumor metastasis is unclear. Beavis et al. evaluated the efficacy of A2A and A2B adenosine receptor antagonists in inhibiting the metastasis of tumors expressing CD73, either endogenously or ectopically. They demonstrate distinct mechanisms whereby A2A versus A2B adenosine receptors could contribute to CD73(+) tumor metastasis. As A2Areceptor (R)/A2BR antagonists have been tested in clinical trials in other disease settings, this study highlights the potential therapeutic application of an A2AR/A2BR blockade strategy for treatment of CD73(+) metastatic tumors.
MeSH Terms
5'-Nucleotidase/immunology
Animals
Humans
Killer Cells, Natural/immunology
Neoplasms, Experimental/immunology
Receptor, Adenosine A2A/immunology
Chemicals
Receptor, Adenosine A2A
5'-Nucleotidase
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Qin Lei
Robert H. Lurie Comprehensive Cancer Center, Department of Medicine-Division of Hematology/Oncology, Northwestern University Feinberg School of Medicine, 300 E Superior Street-Tarry 13-705, Chicago, IL 60611, USA.
Thompson Linda F
Kuzel Timothy M
Zhang Bin
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