Glucose Oncometabolism of Esophageal Cancer

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.

Cite this article as:

Hochwald S. Jason and Zhang Jianliang, Glucose Oncometabolism of Esophageal Cancer, Anti-Cancer Agents in Medicinal Chemistry 2017; 17 (3) . https://dx.doi.org/10.2174/1871520616666160627092716