Journal
CANCER RESEARCH
Volume 70, Issue 1, Pages 89-98Publisher
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/0008-5472.CAN-09-2970
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Funding
- National Natural Science Foundation of China [30771967, 30872315]
- Ministry of Science and Technology of the People's Republic of China [06C26211200695, 2008AA02Z129, 2006AA020502]
- Tianjin Municipal Science and Technology Commission [07JCZDJC03300, 06ZHCXSH04800]
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Dendritic cell (DC) function is negatively affected by tumors and tumor-derived factors, but little is known about the underlying mechanisms. Here, we show that intracellular SOCS3 in DCs binds to pyruvate kinase type M2 (M2-PK), which plays a critical role in ATP production through glycolysis. The interaction of SOCS3 with M2-PK reduced ATP production and impaired DC-based immunotherapy against tumors. Thus, SOCS3, which has been shown to be upregulated by tumor-derived factors, interacts with M2-PK to decrease ATP production, causing DC dysfunction. These dysfunctional DCs have a reduced ability to present antigens. Alteration of DC metabolism mediated by SOCS3 represents a novel mechanism for DC dysfunction in the tumor microenvironment. Cancer Res; 70(1); 89-98. (C)2010 AACR.
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