Requirement of NK cells for selective A2A receptor blockade to suppress CD73+ tumor metastasis

Lei Qin, Linda F. Thompson, Timothy M. Kuzel, Bin Zhang*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

8 Scopus citations

Abstract

Evaluation of: Beavis PA, Divisekera U, Paget C et al. Blockade of A 2A 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 A 2B 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 A 2Areceptor (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.

Original languageEnglish (US)
Pages (from-to)19-21
Number of pages3
JournalImmunotherapy
Volume6
Issue number1
DOIs
StatePublished - Jan 2014

Keywords

  • CD73
  • NK cell
  • adenosine receptor
  • ecto-5́-nucleotidase
  • metastasis

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Oncology

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