The role of p53 in glucose metabolism

被引:70
作者
Cheung, Eric C. [1 ]
Vousden, Karen H. [1 ]
机构
[1] Beatson Inst Canc Res, Glasgow G61 1BD, Lanark, Scotland
基金
加拿大健康研究院;
关键词
APOPTOSIS-INDUCING FACTOR; TUMOR-SUPPRESSOR P53; CANCER-CELLS; MITOCHONDRIAL DYSFUNCTION; SUCCINATE-DEHYDROGENASE; RESPONSE ELEMENTS; CYTOCHROME-C; EXPRESSION; GLYCOLYSIS; GROWTH;
D O I
10.1016/j.ceb.2009.12.006
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The p53 protein functions to prevent tumour development by inhibiting the outgrowth of stressed or damaged cells. In addition to well established functions to block cell proliferation, recent studies have revealed a role for p53 in the regulation of pathways involved in glucose metabolism. The metabolic functions of p53 resist the shift to glycolysis that is characteristically seen in cancers, and also help cells adapt to and survive limited periods of metabolic stress. Such activities of p53 would not only help to prevent cancer development, but might also contribute to non-tumour related roles for p53, such as in the regulation of longevity. These new functions of p53 are providing interesting possibilities for the development of novel therapies.
引用
收藏
页码:186 / 191
页数:6
相关论文
共 55 条
[31]   Hexokinase-mitochondria interaction mediated by Akt is required to inhibit apoptosis in the presence or absence of Bax and Bak [J].
Majewski, N ;
Nogueira, V ;
Bhaskar, P ;
Coy, PE ;
Skeen, JE ;
Gottlob, K ;
Chandel, NS ;
Thompson, CB ;
Robey, RB ;
Hay, N .
MOLECULAR CELL, 2004, 16 (05) :819-830
[32]   Glucose catabolism in cancer cells - The type II hexokinase promoter contains functionally active response elements for the tumor suppressor p53 [J].
Mathupala, SP ;
Heese, C ;
Pedersen, PL .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1997, 272 (36) :22776-22780
[33]   p53 regulates mitochondrial respiration [J].
Matoba, Satoaki ;
Kang, Ju-Gyeong ;
Patino, Willmar D. ;
Wragg, Andrew ;
Boehm, Manfred ;
Gavrilova, Oksana ;
Hurley, Paula J. ;
Bunz, Fred ;
Hwang, Paul M. .
SCIENCE, 2006, 312 (5780) :1650-1653
[34]   Pyruvate dehydrogenase complex activity controls metabolic and malignant phenotype in cancer cells [J].
McFate, Thomas ;
Mohyeldin, Ahmed ;
Lu, Huasheng ;
Thakar, Jay ;
Henriques, Jeremy ;
Halim, Nader D. ;
Wu, Hong ;
Schell, Michael J. ;
Tsang, Tsz Mon ;
Teahan, Orla ;
Zhou, Shaoyu ;
Califano, Joseph A. ;
Jeoung, Nam Ho ;
Harris, Robert A. ;
Verma, Ajay .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2008, 283 (33) :22700-22708
[35]   Dichloroacetate (DCA) as a potential metabolic-targeting therapy for cancer [J].
Michelakis, E. D. ;
Webster, L. ;
Mackey, J. R. .
BRITISH JOURNAL OF CANCER, 2008, 99 (07) :989-994
[36]   Overexpression of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase-4 in the human breast and colon malignant tumors [J].
Minchenko, OH ;
Ochiai, A ;
Opentanova, IL ;
Ogura, T ;
Minchenko, DO ;
Caro, J ;
Komisarenko, SV ;
Esumi, H .
BIOCHIMIE, 2005, 87 (11) :1005-1010
[37]   c-Myc activates multiple metabolic networks to generate substrates for cell-cycle entry [J].
Morrish, F. ;
Isern, N. ;
Sadilek, M. ;
Jeffrey, M. ;
Hockenbery, D. M. .
ONCOGENE, 2009, 28 (27) :2485-2491
[38]   Reactive Oxygen Species-independent Oxidation of Thioredoxin in Hypoxia INACTIVATION OF RIBONUCLEOTIDE REDUCTASE AND REDOX-MEDIATED CHECKPOINT CONTROL [J].
Muniyappa, Harish ;
Song, Shiwei ;
Mathews, Christopher K. ;
Das, Kumuda C. .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2009, 284 (25) :17069-17081
[39]   HIF-1 mediates adaptation to hypoxia by actively downregulating mitochondrial oxygen consumption [J].
Papandreou, I ;
Cairns, RA ;
Fontana, L ;
Lim, AL ;
Denko, NC .
CELL METABOLISM, 2006, 3 (03) :187-197
[40]   Cooperation and competition in the evolution of ATP-producing pathways [J].
Pfeiffer, T ;
Schuster, S ;
Bonhoeffer, S .
SCIENCE, 2001, 292 (5516) :504-507