Energy metabolism in tumor cells

@article{MorenoSnchez2007EnergyMI,
  title={Energy metabolism in tumor cells},
  author={Rafael Moreno-S{\'a}nchez and Sara Rodr{\'i}guez-Enr{\'i}quez and {\'A}lvaro Mar{\'i}n-Hern{\'a}ndez and Emma Saavedra},
  journal={The FEBS Journal},
  year={2007},
  volume={274}
}
In early studies on energy metabolism of tumor cells, it was proposed that the enhanced glycolysis was induced by a decreased oxidative phosphorylation. Since then it has been indiscriminately applied to all types of tumor cells that the ATP supply is mainly or only provided by glycolysis, without an appropriate experimental evaluation. In this review, the different genetic and biochemical mechanisms by which tumor cells achieve an enhanced glycolytic flux are analyzed. Furthermore, the… 
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References

SHOWING 1-10 OF 228 REFERENCES
Deviant energetic metabolism of glycolytic cancer cells.
Contribution by different fuels and metabolic pathways to the total ATP turnover of proliferating MCF-7 breast cancer cells.
TLDR
Using an innovative system, the total ATP turnover of the MCF-7 breast cancer cell line is measured, the contributions to this turnover by oxidative and glycolytic ATP production and the contributes to the oxidative component by glucose, lactate, glutamine, palmitate and oleate are measured.
Control of cellular proliferation by modulation of oxidative phosphorylation in human and rodent fast-growing tumor cells.
Substrate oxidation and ATP supply in AS-30D hepatoma cells.
TLDR
The data indicated that AS-30D hepatoma cells had a predominantly oxidative and not a glycolytic type of metabolism.
p53 Regulates Mitochondrial Respiration
TLDR
It is shown that p53, one of the most frequently mutated genes in cancers, modulates the balance between the utilization of respiratory and glycolytic pathways, and Synthesis of Cytochrome c Oxidase 2 (SCO2) is identified as the downstream mediator of this effect.
Energy Substrate Modulates Mitochondrial Structure and Oxidative Capacity in Cancer Cells
TLDR
The data show that the defective mitochondrial system described in cancer cells can be dramatically improved by solely changing substrate availability and that HeLa cells can adapt their mitochondrial network structurally and functionally to derive energy by glutaminolysis only.
Regulation of cellular energy metabolism: the Crabtree effect.
Oncogenes in Tumor Metabolism, Tumorigenesis, and Apoptosis
The ability of cancer cells to overproduce lactic acid aerobically was recognized by Warburg about seven decades ago, although its molecular basis has been elusive. Increases in glucose transport and…
Deregulation of Glucose Transporter 1 and Glycolytic Gene Expression by c-Myc*
TLDR
Findings suggest that overexpression of the c-Myc oncoprotein deregulates glycolysis through the activation of several components of the glucose metabolic pathway.
Effect of Extracellular AMP on Cell Proliferation and Metabolism of Breast Cancer Cell Lines with High and Low Glycolytic Rates*
TLDR
In differentiated tissues, such as muscle and brain, increased adenosine monophosphate (AMP) levels stimulate glycolytic flux rates and inhibits cell proliferation as well as NAD and NADH synthesis in both MCF-7 and MDA-MB-453 cells.
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