Is Cancer a Metabolic Disease?

被引:179
作者
Coller, Hilary A. [1 ]
机构
[1] Princeton Univ, Dept Mol Biol, Princeton, NJ 08544 USA
关键词
PYRUVATE-DEHYDROGENASE KINASE; POSITRON-EMISSION-TOMOGRAPHY; SMALL-MOLECULE INHIBITION; ENDOTHELIAL GROWTH-FACTOR; HIGH LACTATE LEVELS; INDUCIBLE FACTOR-I; GLUCOSE-METABOLISM; AEROBIC GLYCOLYSIS; CELL-GROWTH; C-MYC;
D O I
10.1016/j.ajpath.2013.07.035
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
Although cancer has historically been viewed as a disorder of proliferation, recent evidence has suggested that it should also be considered a metabolic disease. Growing tumors rewire their metabolic programs to meet and even exceed the bioenergetic and biosynthetic demands of continuous cell growth. The metabolic profile observed in cancer cells often includes increased consumption of glucose and glutamine, increased glycolysis, changes in the use of metabolic enzyme isoforms, and increased secretion of lactate. Oncogenes and tumor suppressors have been discovered to have roles in cancer-associated changes in metabolism as well. The metabolic profile of tumor cells has been suggested to reflect the rapid proliferative rate. Cancer-associated metabolic changes may also reveal the importance of protection against reactive oxygen species or a role for secreted lactate in the tumor microenvironment. This article reviews recent research in the field of cancer metabolism, raising the following questions: Why do cancer cells shift their metabolism in this way? Are the changes in metabolism in cancer cells a consequence of the changes in proliferation or a driver of cancer progression? Can cancer metabolism be targeted to benefit patients?
引用
收藏
页码:4 / 17
页数:14
相关论文
共 132 条
  • [81] The bioenergetics of cancer: Is glycolysis the main ATP supplier in all tumor cells?
    Moreno-Sanchez, Rafael
    Rodriguez-Enriquez, Sara
    Saavedra, Emma
    Marin-Hernandez, Alvaro
    Carlos Gallardo-Perez, Juan
    [J]. BIOFACTORS, 2009, 35 (02) : 209 - 225
  • [82] MYC oncogenes and human neoplastic disease
    Nesbit, CE
    Tersak, JM
    Prochownik, EV
    [J]. ONCOGENE, 1999, 18 (19) : 3004 - 3016
  • [83] THE ROLE OF HIGH-RATES OF GLYCOLYSIS AND GLUTAMINE UTILIZATION IN RAPIDLY DIVIDING CELLS
    NEWSHOLME, EA
    CRABTREE, B
    ARDAWI, MSM
    [J]. BIOSCIENCE REPORTS, 1985, 5 (05) : 393 - 400
  • [84] Stromal fibroblasts present in invasive human breast carcinomas promote tumor growth and angiogenesis through elevated SDF-1/CXCL12 secretion
    Orimo, A
    Gupta, PB
    Sgroi, DC
    Arenzana-Seisdedos, F
    Delaunay, T
    Naeem, R
    Carey, VJ
    Richardson, AL
    Weinberg, RA
    [J]. CELL, 2005, 121 (03) : 335 - 348
  • [85] Accelerated publication -: Deregulation of glucose transporter 1 and glycolytic gene expression by c-Myc
    Osthus, RC
    Shim, H
    Kim, S
    Li, Q
    Reddy, R
    Mukherjee, M
    Xu, Y
    Wonsey, D
    Lee, LA
    Dang, CV
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (29) : 21797 - 21800
  • [86] Hexokinase II: The integration of energy metabolism and control of apoptosis
    Pastorino, JG
    Hoek, JB
    [J]. CURRENT MEDICINAL CHEMISTRY, 2003, 10 (16) : 1535 - 1551
  • [87] Warburg, me and hexokinase 2: Multiple discoveries of key molecular events underlying one of cancers' most common phenotypes, the "Warburg Effect", i.e., elevated glycolysis in the presence of oxygen
    Pedersen, Peter L.
    [J]. JOURNAL OF BIOENERGETICS AND BIOMEMBRANES, 2007, 39 (03) : 211 - 222
  • [88] The prognostic value of CD147/EMMPRIN is associated with monocarboxylate transporter 1 co-expression in gastric cancer
    Pinheiro, Celine
    Longatto-Filho, Adhemar
    Simoes, Kleber
    Jacob, Carlos Eduardo
    Caldas Bresciani, Claudio Jose
    Zilberstein, Bruno
    Cecconello, Ivan
    Ferreira Alves, Venancio Avancini
    Schmitt, Fernando
    Baltazar, Fatima
    [J]. EUROPEAN JOURNAL OF CANCER, 2009, 45 (13) : 2418 - 2424
  • [89] Pinheiro C, 2009, DIS MARKERS, V26, P97, DOI [10.1155/2009/169678, 10.3233/DMA-2009-0596]
  • [90] Podoloff Donald A, 2007, J Natl Compr Canc Netw, V5 Suppl 1, pS1