| Literature DB >> 26271140 |
Abbas Shafaee1, Davood Zarei Dastyar2, Jalil Pirayesh Islamian3, Milad Hatamian4.
Abstract
Interest in targeting cancer metabolism has been renewed in recent years with the discovery that many cancer related pathways have a profound effect on metabolism and that many tumors become dependent on specific metabolic processes. Accelerated glucose uptake during anaerobic glycolysis and loss of regulation between glycolytic metabolism and respiration, are the major metabolic changes found in malignant cells. The non-metabolizable glucose analog, 2-deoxy-D-glucose inhibits glucose synthesis and adenosine triphosphate production. The adenosine monophosphate-activated protein kinase (AMPK) is a key sensor of cellular energy and AMPK is a potential target for cancer prevention and/or treatment. Metformin is an activator of AMPK which inhibits protein synthesis and gluconeogenesis during cellular stress. This article reviews the status of clinical and laboratory researches exploring targeted therapies via metabolic pathways for treatment of esophageal cancer.Entities:
Keywords: AMPK; Esophageal cancer; Gluconeogenesis; Metformin; Targeted therapy
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Year: 2015 PMID: 26271140 DOI: 10.1016/j.metabol.2015.07.005
Source DB: PubMed Journal: Metabolism ISSN: 0026-0495 Impact factor: 8.694