Title:Glucose Oncometabolism of Esophageal Cancer
Volume: 17
Issue: 3
Author(s): Jason S. Hochwald and Jianliang Zhang
Affiliation:
Keywords:
Tumor metabolism, glycolysis, mitochondria, altered genes, inhibitors, glucose dependence.
Abstract: Metabolic reprograming contributes to esophageal tumorigenesis. A better understanding of how esophageal
cancer (EC) cells reactivate primitive signaling to retain glucose metabolism under unfavorable conditions is essential for
the development of therapeutic interventions to treat EC. Current achievements in the field of EC glucose metabolism
have been critically reviewed to address several fundamental questions. These include: 1) the association of abnormal
glucose metabolism and EC risk; 2) alterations of genes and/or proteins that contribute to glucose oncometabolism in
EC; 3) signal transduction pathways that promote EC consumption of glucose; and, 4) targeting the glycolytic element
or the EC dependency on excessive glucose consumption to prevent growth of EC caused by different genomic
changes.
