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. Author manuscript; available in PMC: 2017 Feb 9.
Published in final edited form as: Postdoc J. 2017 Jan;5(1):14–28. doi: 10.14304/surya.jpr.v5n1.4

Figure 1. Regulation of HNSCC glycolysis.

Figure 1

HNSCC tumors are more dependent on glycolysis. This model represents the regulation of glycolysis in HNSCC. Mutation in p53 activates HIF-1α, which regulates GLUT-1, HK-II and LDH-A expression in HNSCC. The overexpression of TKTL1 in HNSCC increases lactate production by increasing fructose-6-phosphate and glyceraldehyde-3-phosphate activity. Overexpression of MCTs export lactate out from the cells to protect cell damage as of the high accumulation of lactate decreases pH in intracellular environment.