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Immunoregulatory Protein B7-H3 Reprograms Glucose Metabolism in Cancer Cells by ROS-Mediated Stabilization of HIF1α.

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机构： [1]Center for Cell Death and Metabolism, Mitchell Cancer Institute,University of South Alabama, Mobile, Alabama [2]Department of Biochemistryand Molecular Biology,West China School of Preclinical andForensic Medicine, Sichuan University, Chengdu, China [3]Departmentof Neuroscience, University of Minnesota, Minneapolis, Minnesota [4]Department of Tumor Biology, Norwegian Radium Hospital, OsloUniversity Hospital, and Institute for Clinical Medicine, Faculty ofMedicine, University of Oslo, Oslo, Norway [5]Department of Biochemistryand Molecular Biology, University of South Alabama, Mobile,Alabama

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B7-H3 is a member of B7 family of immunoregulatory transmembrane glycoproteins expressed by T cells. While B7-H3 overexpression is associated with poor outcomes in multiple cancers, it also has immune-independent roles outside T cells and its precise mechanistic contributions to cancer are unclear. In this study, we investigated the role of B7-H3 in metabolic reprogramming of cancer cells in vitro and in vivo We found that B7-H3 promoted the Warburg effect, evidenced by increased glucose uptake and lactate production in B7-H3-expressing cells. B7-H3 also increased the protein levels of HIF1α and its downstream targets, LDHA and PDK1, key enzymes in the glycolytic pathway. Furthermore, B7-H3 promoted reactive oxygen species-dependent stabilization of HIF1α by suppressing the activity of the stress-activated transcription factor Nrf2 and its target genes, including the antioxidants SOD1, SOD2, and PRX3. Metabolic imaging of human breast cancer xenografts in mice confirmed that B7-H3 enhanced tumor glucose uptake and tumor growth. Together, our results illuminate the critical immune-independent contributions of B7-H3 to cancer metabolism, presenting a radically new perspective on B7 family immunoregulatory proteins in malignant progression. Cancer Res; 76(8); 2231-42. ©2016 AACR. ©2016 American Association for Cancer Research.

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出版当年[2016]版：

大类 | 1 区

医学

小类 | 1 区肿瘤学

最新[2023]版：

大类 | 1 区

医学

小类 | 2 区肿瘤学

第一作者：

第一作者机构： [1]Center for Cell Death and Metabolism, Mitchell Cancer Institute,University of South Alabama, Mobile, Alabama

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通讯机构： [1]Center for Cell Death and Metabolism, Mitchell Cancer Institute,University of South Alabama, Mobile, Alabama [2]Department of Biochemistryand Molecular Biology,West China School of Preclinical andForensic Medicine, Sichuan University, Chengdu, China [4]Department of Tumor Biology, Norwegian Radium Hospital, OsloUniversity Hospital, and Institute for Clinical Medicine, Faculty ofMedicine, University of Oslo, Oslo, Norway [5]Department of Biochemistryand Molecular Biology, University of South Alabama, Mobile,Alabama [*1]Mitchell Cancer Institute, University of South Alabama, 1660 Springhill Avenue, Mobile, AL 366604 [*2]Department of Biochemistry & Molecular Biology, West China School of Preclinical and Forensic Medicine, Sichuan University, Chengdu, China. [*3]Department of Tumor Biology, Institute for Cancer Research, Oslo, Norway.

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