Dysregulation of glucose transport, glycolysis, TCA cycle and glutaminolysis by oncogenes and tumor suppressors in cancer cells

被引:241
作者
Chen, Jin-Qiang [1 ,2 ]
Russo, Jose [1 ]
机构
[1] Fox Chase Canc Ctr, Breast Canc Res Lab, Philadelphia, PA 19111 USA
[2] Gold Belt Falcon LLC, Chesapeake, VA 23360 USA
来源
BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER | 2012年 / 1826卷 / 02期
关键词
p53; c-Myc; Glucose transporter; Glycolysis; TCA cycle; Glutaminolysis; PYRUVATE-DEHYDROGENASE KINASE; POSITRON-EMISSION-TOMOGRAPHY; INHIBITION-RESISTANT FORM; PENTOSE-PHOSPHATE PATHWAY; ENERGY-METABOLISM; MOLECULAR-CLONING; GLUT1; EXPRESSION; BREAST-CANCER; SDHD GENE; P53-INDUCIBLE REGULATOR;
D O I
10.1016/j.bbcan.2012.06.004
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
A common set of functional characteristics of cancer cells is that cancer cells consume a large amount of glucose, maintain high rate of glycolysis and convert a majority of glucose into lactic acid even in the presence of oxygen compared to that of normal cells (Warburg's Effects). In addition, cancer cells exhibit substantial alterations in several energy metabolism pathways including glucose transport, tricarboxylic acid (TCA) cycle, glutaminolysis, mitochondrial respiratory chain oxidative phosphorylation and pentose phosphate pathway (PPP). In the present work, we focused on reviewing the current knowledge about the dysregulation of the proteins/enzymes involved in the key regulatory steps of glucose transport, glycolysis. TCA cycle and glutaminolysis by several oncogenes including c-Myc and hypoxia inducible factor-1 (HIF-1) and tumor suppressor, p53, in cancer cells. The dysregulation of glucose transport and energy metabolism pathways by oncogenes and lost functions of the tumor suppressors have been implicated as important biomarkers for cancer detection and as valuable targets for the development of new anticancer therapies. (C) 2012 Elsevier B.V. All rights reserved.
引用
收藏
页码:370 / 384
页数:15
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