Inhibition of tumor energy pathways for targeted esophagus cancer therapy.

Autor: Shafaee A; Department of Radiology, School of Paramedicine, Tabriz University of Medical Sciences, Tabriz, Iran., Dastyar DZ; Department of Medical Radiation Science, School of Paramedicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran., Islamian JP; Department of Medical Physics, School of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran. Electronic address: pirayeshj@gmail.com., Hatamian M; Department of Medical Physics, School of Medical Sciences, Tarbiat Modares University, Tehran, Iran.
Jazyk: angličtina
Zdroj: Metabolism: clinical and experimental [Metabolism] 2015 Oct; Vol. 64 (10), pp. 1193-8. Date of Electronic Publication: 2015 Jul 17.
DOI: 10.1016/j.metabol.2015.07.005
Abstrakt: 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.
(Copyright © 2015 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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