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10.1080/2162402X.2017.1320011

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suck abstract from ncbi


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pmid28680754
      Oncoimmunology 2017 ; 6 (6 ): e1320011
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  • CD39/CD73 upregulation on myeloid-derived suppressor cells via TGF-?-mTOR-HIF-1 signaling in patients with non-small cell lung cancer #MMPMID28680754
  • Li J ; Wang L ; Chen X ; Li L ; Li Y ; Ping Y ; Huang L ; Yue D ; Zhang Z ; Wang F ; Li F ; Yang L ; Huang J ; Yang S ; Li H ; Zhao X ; Dong W ; Yan Y ; Zhao S ; Huang B ; Zhang B ; Zhang Y
  • Oncoimmunology 2017[]; 6 (6 ): e1320011 PMID28680754 show ga
  • CD39/CD73-adenosine pathway has been recently defined as an important tumor-induced immunosuppressive mechanism. We here documented a fraction of CD11b(+)CD33(+) myeloid-derived suppressor cells (MDSCs) in peripheral blood and tumor tissues from non-small cell lung cancer (NSCLC) patients expressed surface ectonucleotidases CD39 and CD73. Tumor TGF-? stimulated CD39 and CD73 expression, thereby inhibited T cell and NK cell activity, and protected tumor cells from the cytotoxic effect of chemotherapy through ectonucleotidase activity. Mechanistically, TGF-? triggered phosphorylation of mammalian target of rapamycin, and subsequently activated hypoxia-inducible factor-1? (HIF-1?) that induced CD39/CD73 expression on MDSCs. CD39 and CD73 on MDSCs, therefore, link their immunosuppressive and chemo-protective effects to NSCLC progression, providing novel targets for chemo-immunotherapeutic intervention.
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