The Role of Dysregulated Glucose Metabolism in Epithelial Ovarian Cancer

Figure 1

Summary diagram of factors hypothesized to link hyperglycemia to the development of epithelial ovarian cancer. Hyperglycemia, leading to hyperinsulinemia and inflammation, underlies the development of parallel pathologies affecting growth and death signaling, formation of reactive species, and angiogenesis. Together, these aberrant signals converge on a hyperproliferative phenotype that may promote or initiate the development of cancer. Possible therapeutic approaches, including the novel application of antidiabetic drugs, are shown in green. Abbreviations: TZDs, thiazolidinedoines; GLUTs, facilitative glucose transporters; ROS, reactive oxygen species; NSAIDs, nonsteroidal antiinflammatory drugs; AGE-RAGE, advanced glycation end product receptor complex; IR-A and IR-B, insulin receptor isoforms A and B; IGF(R), insulin-like growth factor (receptor); cdk, cyclin-dependant kinase; TSP-1, thrombospondin-1; HIF-1𝛼, hypoxia-inducible factor alpha; NF-κB, nuclear factor kappa B; VEGF, vascular endothelial growth factor.