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. Author manuscript; available in PMC: 2017 Apr 15.
Published in final edited form as: Cancer Res. 2016 Apr 5;76(8):2231–2242. doi: 10.1158/0008-5472.CAN-15-1538

Figure 7. Model for the role of B7-H3 regulating glucose metabolism.

Figure 7

Through unknown mechanisms, B7-H3 suppresses Nrf2 transcriptional activity, which in turn reduces transcription of the antioxidant enzymes SOD1, SOD2 and PRX3. As a result, B7-H3 overexpression leads to increased ROS in cancer cells. B7-H3-induced ROS stabilizes HIF-1α thus increasing the expression of glycolytic enzymes LDHA and PDK1, which promotes pyruvate conversion into lactate while inhibiting pyruvate flux through the TCA cycle. As a result, B7-H3 promotes aerobic glycolysis in cancer cells and therefore tumor growth.