The bioenergetics of cancer: Is glycolysis the main ATP supplier in all tumor cells?

被引：100

作者：

Moreno-Sanchez, Rafael ^{[1
]}

Rodriguez-Enriquez, Sara ^{[1
]}

Saavedra, Emma ^{[1
]}

Marin-Hernandez, Alvaro ^{[1
]}

Carlos Gallardo-Perez, Juan ^{[1
]}

机构：

[1] Inst Nacl Cardiol, Dept Bioquim, Mexico City 14080, DF, Mexico

来源：

BIOFACTORS | 2009年 / 35卷 / 02期

关键词：

glycolysis; oxidative phosphorylation; mitochondrial function; PET; metabolic control analysis; FACILITATIVE GLUCOSE TRANSPORTERS; POSITRON-EMISSION-TOMOGRAPHY; ENDOTHELIAL GROWTH-FACTOR; CYTOCHROME-C-OXIDASE; SYSTEM IN-VITRO; MITOCHONDRIAL-DNA; OXIDATIVE-PHOSPHORYLATION; HEPATOCELLULAR-CARCINOMA; ENERGY-METABOLISM; MALIGNANT-TRANSFORMATION;

D O I：

10.1002/biof.31

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：

The molecular mechanisms by which tumor cells achieve an enhanced glycolytic flux and, presumably, a decreased oxidative phosphorylation are analyzed. As the O-2 concentration in hypoxic regions of tumors seems not limiting for oxidative phosphorylation, the role of this mitochondrial pathway in the ATP supply is re-evaluated. Drugs that inhibit glycoysis and oxidative phosphorylation are analyzed for their specificity toward tumor cells and effect on proliferation. The energy metabolism mechanisms involved in the use of positron emission tomography are revised and updated. It is proposed that energy metabolism may be an alternative therapeutic target for both hypoxic (glycolytic) and oxidative tumors. (C) 2009 International Union of Biochemistry and Molecular Biology, Inc. Volume 35, Number 2, March/April 2009, Pages 209-225 . E-mail: rafael.moreno@cardiologia.org.mx or more morenosanchez@hotmail.com

引用

页码：209 / 225

页数：17

共 152 条

[1] Genes of glycolysis are ubiquitously overexpressed in 24 cancer classes [J].

Altenberg, B ;

Greulich, KO .

GENOMICS, 2004, 84 (06) :1014-1020

[2] c-Myc overexpression sensitises colon cancer cells to camptothecin-induced apoptosis [J].

Arango, D ;

Mariadason, JM ;

Wilson, AJ ;

Yang, W ;

Corner, GA ;

Nicholas, C ;

Aranes, MJ ;

Augenlicht, LH .

BRITISH JOURNAL OF CANCER, 2003, 89 (09) :1757-1765

[3]

BALINSKY D, 1984, JNCI-J NATL CANCER I, V72, P217

[4] ISOENZYMES OF HEXOKINASE IN DEVELOPING, NORMAL AND NEOPLASTIC HUMAN-BRAIN [J].

BENNETT, MJ ;

TIMPERLEY, WR ;

TAYLOR, CB ;

HILL, AS .

EUROPEAN JOURNAL OF CANCER, 1978, 14 (02) :189-193

[5]

BERBERAT P, 2004, CURR CANCER DRUG TAR, V4, P355

[6]

BESAAD K, 2006, CELL, V126, P8180

[7] A mitochondria-K+ channel axis is suppressed in cancer and its normalization promotes apoptosis and inhibits cancer growth [J].

Bonnet, Sebastien ;

Archer, Stephen L. ;

Allalunis-Turner, Joan ;

Haromy, Alois ;

Beaulieu, Christian ;

Thompson, Richard ;

Lee, Christopher T. ;

Lopaschuk, Gary D. ;

Puttagunta, Lakshmi ;

Bonnet, Sandra ;

Harry, Gwyneth ;

Hashimoto, Kyoko ;

Porter, Christopher J. ;

Andrade, Miguel A. ;

Thebaud, Bernard ;

Michelakis, Evangelos D. .

CANCER CELL, 2007, 11 (01) :37-51

[8] p53 and its isoforms in cancer [J].

Bourdon, J-C .

BRITISH JOURNAL OF CANCER, 2007, 97 (03) :277-282

[9] Mitochondrial mutations in cancer [J].

Brandon, M. ;

Baldi, P. ;

Wallace, D. C. .

ONCOGENE, 2006, 25 (34) :4647-4662

[10] A highly sensitive biocompatible spin probe for imaging of oxygen concentration in tissues [J].

Bratasz, Anna ;

Kulkarni, Aditi C. ;

Kuppusamy, Periannan .

BIOPHYSICAL JOURNAL, 2007, 92 (08) :2918-2925

← 1 2 3 4 5 6 7 8 9 10 →