PMID- 24513530
OWN - NLM
STAT- MEDLINE
DCOM- 20150715
LR  - 20220316
IS  - 1878-5875 (Electronic)
IS  - 1357-2725 (Linking)
VI  - 50
DP  - 2014 May
TI  - Who controls the ATP supply in cancer cells? Biochemistry lessons to understand 
      cancer energy metabolism.
PG  - 10-23
LID - S1357-2725(14)00042-9 [pii]
LID - 10.1016/j.biocel.2014.01.025 [doi]
AB  - Applying basic biochemical principles, this review analyzes data that contrasts 
      with the Warburg hypothesis that glycolysis is the exclusive ATP provider in 
      cancer cells. Although disregarded for many years, there is increasing 
      experimental evidence demonstrating that oxidative phosphorylation (OxPhos) makes 
      a significant contribution to ATP supply in many cancer cell types and under a 
      variety of conditions. Substrates oxidized by normal mitochondria such as amino 
      acids and fatty acids are also avidly consumed by cancer cells. In this regard, 
      the proposal that cancer cells metabolize glutamine for anabolic purposes without 
      the need for a functional respiratory chain and OxPhos is analyzed considering 
      thermodynamic and kinetic aspects for the reductive carboxylation of 
      2-oxoglutarate catalyzed by isocitrate dehydrogenase. In addition, metabolic 
      control analysis (MCA) studies applied to energy metabolism of cancer cells are 
      reevaluated. Regardless of the experimental/environmental conditions and the rate 
      of lactate production, the flux-control of cancer glycolysis is robust in the 
      sense that it involves the same steps: glucose transport, hexokinase, 
      hexosephosphate isomerase and glycogen degradation, all at the beginning of the 
      pathway; these steps together with phosphofructokinase 1 also control glycolysis 
      in normal cells. The respiratory chain complexes exert significantly higher 
      flux-control on OxPhos in cancer cells than in normal cells. Thus, determination 
      of the contribution of each pathway to ATP supply and/or the flux-control 
      distribution of both pathways in cancer cells is necessary in order to identify 
      differences from normal cells which may lead to the design of rational 
      alternative therapies that selectively target cancer energy metabolism.
CI  - Copyright (c) 2014 Elsevier Ltd. All rights reserved.
FAU - Moreno-Sanchez, Rafael
AU  - Moreno-Sanchez R
AD  - Instituto Nacional de Cardiologia, Departamento de Bioquimica, Tlalpan, Mexico 
      D.F., Mexico. Electronic address: rafael.moreno@cardiologia.org.mx.
FAU - Marin-Hernandez, Alvaro
AU  - Marin-Hernandez A
AD  - Instituto Nacional de Cardiologia, Departamento de Bioquimica, Tlalpan, Mexico 
      D.F., Mexico.
FAU - Saavedra, Emma
AU  - Saavedra E
AD  - Instituto Nacional de Cardiologia, Departamento de Bioquimica, Tlalpan, Mexico 
      D.F., Mexico.
FAU - Pardo, Juan P
AU  - Pardo JP
AD  - Universidad Nacional Autonoma de Mexico, Facultad de Medicina, Departamento de 
      Bioquimica, Mexico D.F., Mexico.
FAU - Ralph, Stephen J
AU  - Ralph SJ
AD  - School of Medical Sciences, Griffith University, Gold Coast Campus, Qld, 
      Australia.
FAU - Rodriguez-Enriquez, Sara
AU  - Rodriguez-Enriquez S
AD  - Instituto Nacional de Cardiologia, Departamento de Bioquimica, Tlalpan, Mexico 
      D.F., Mexico; Instituto Nacional de Cancerologia, Laboratorio de Medicina 
      Translacional, Tlalpan, Mexico D.F., Mexico.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20140207
PL  - Netherlands
TA  - Int J Biochem Cell Biol
JT  - The international journal of biochemistry & cell biology
JID - 9508482
RN  - 0RH81L854J (Glutamine)
RN  - 8L70Q75FXE (Adenosine Triphosphate)
SB  - IM
MH  - Adenosine Triphosphate/*metabolism
MH  - Animals
MH  - Biological Transport
MH  - Energy Metabolism
MH  - Glutamine/metabolism
MH  - Humans
MH  - Neoplasms/*metabolism
MH  - Oxidative Phosphorylation
OTO - NOTNLM
OT  - Cancer glutamine metabolism
OT  - Isocitrate dehydrogenase
OT  - Oxidative phosphorylation
OT  - Warburg hypothesis
EDAT- 2014/02/12 06:00
MHDA- 2015/07/16 06:00
CRDT- 2014/02/12 06:00
PHST- 2013/10/21 00:00 [received]
PHST- 2014/01/21 00:00 [revised]
PHST- 2014/01/26 00:00 [accepted]
PHST- 2014/02/12 06:00 [entrez]
PHST- 2014/02/12 06:00 [pubmed]
PHST- 2015/07/16 06:00 [medline]
AID - S1357-2725(14)00042-9 [pii]
AID - 10.1016/j.biocel.2014.01.025 [doi]
PST - ppublish
SO  - Int J Biochem Cell Biol. 2014 May;50:10-23. doi: 10.1016/j.biocel.2014.01.025. 
      Epub 2014 Feb 7.