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. 2017 Sep 19;8(60):100989–101004. doi: 10.18632/oncotarget.21054

Figure 7. Model summarizing aerobic training effects on breast tumor biological pathways in the C3(1)SV40Tag-p16-luc model.

Figure 7

A. Aerobic training effects on breast tumor biological pathways in the C3(1)SV40Tag-p16-luc mouse model. Aerobic training in mice leads to stabilization of Hif1-α protein in C3(1)SV40Tag-p16-luc tumors. Hif1-α mediates inhibition of oxidative phosphorylation and citric acid cycle (TCA) through PDK-1 as well as upregulation of glycolysis through Glut-1. Hif1-α also increases fatty acid oxidation (FAO). Together increases in Glut-1 and FAO provide precursors for tumor cell proliferation. B. Aerobic training effects on breast tumor biological pathways with Hif1-α inhibition in the C3(1)SV40Tag-p16-luc mouse model. Hif1-α inhibition by the cardiac glycoside Digoxin prevents upregulation of glycolysis and inhibition of oxidative phosphorylation and TCA. Preventing Hif1-α metabolic reprogramming leads to reduced metabolic dysregulation and tumor growth. C. Model summarizing aerobic training effects on breast tumor biology in EO771 model. Aerobic training in mice decreases Hif1-α in EO771 tumors. Decreased Hif1-α protein alters metabolism in glycerol phosphate and phenylacetate, which may lead to decreased breast cancer cell proliferation through lower precursor formation.