Amoedo 2013 Biosci Rep

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Amoêdo ND, Valencia JP, Rodrigues MF, Galina A, Rumjanek FD (2013) How does the metabolism of tumour cells differ from that of normal cells. Biosci Rep 33:e00080

» PMID: 24079832 Open Access

Amoedo ND, Perez Valencia JA, Rodrigues MF, Galina A, Rumjanek FD (2013) Biosci Rep

Abstract: Tumor cells thrive in environments that would be hostile to their normal cell counterparts. Survival depends on the selection of cell lines that harbor modifications of both, gene regulation that shifts the balance between the cell cycle and apoptosis and those that involve the plasticity of the metabolic machinery. With regards to metabolism, the selected phenotypes usually display enhanced anaerobic glycolysis even in the presence of oxygen, the so called Warburg effect, and anabolic pathways that provide precursors for the synthesis of lipids, proteins and DNA. The review will discuss the original ideas of Otto Warburg and how they initially led to the notion that mitochondria of tumor cells were dysfunctional. Data will be presented to show that not only the organelles are viable and respiring, but that they are key players in tumorigenesis and metastasis. Likewise, interconnecting pathways that stand out in the tumor phenotype and that require intact mitochondria such as glutaminolysis will be addressed. Furthermore, comments will be made as to how the peculiarities of the biochemistry of tumor cells renders them amenable to new forms of treatment by highlighting possible targets for inhibitors. In this respect, a case study describing the effect of a metabolite analogue, the alkylating agent 3-bromopyruvate, on glycolytic enzyme targets will be presented.

Keywords: Energy, Glutamine, Glycolysis, Hypoxia, Lipids, Mitochondria.

O2k-Network Lab: BR Rio de Janeiro Rumjanek FD, BR Rio de Janeiro Galina A, BR Rio de Janeiro Institute Biomedical Chemistry


Labels: MiParea: Respiration, mt-Medicine  Pathology: Cancer 






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