Abstract
Now, at the beginning of a new century, 80 years after Warburgs Nobel prize winning discoveries, we are beginning to make sense of the underlying causes of the well known metabolic phenotype of tumor cells. Building on decades of research to understand the interrelationships between respiration and glycolysis in cancer, the tumor metabolic phenotype can now begin to be understood in a genomic context. With the discovery of hypoxia inducible factor-1 (HIF-1), which is widely overexpressed across a broad range of cancers, modern molecular tools have allowed us to put together the pattern of events that might explain the metabolic differences between tumor and normal cells. HIF-1 controls cellular and systemic responses to oxygen availability and coordinates upregulation of genes involved in many pathways concerned with tumour growth and metabolism including angiogenesis, glucose and energy metabolism, cellular proliferation, differentiation and viability, apoptosis, pH regulation and matrix metabolism. These findings begin to explain how glucose uptake and glycolysis could be up-regulated in cancer cells (through binding to a core DNA recognition sequence) in a co-ordinated and constitutive fashion that may also allow us to elucidate new targets for tumor therapy.
Keywords: tumor metabolic phenotype, genomic era, hif-1, hypoxia inducible factor-1, warburg
Current Molecular Medicine
Title: Understanding the Tumor Metabolic Phenotype in the Genomic Era
Volume: 3 Issue: 1
Author(s): M. Stubbs, C. L. Bashford and J. R. Griffiths
Affiliation:
Keywords: tumor metabolic phenotype, genomic era, hif-1, hypoxia inducible factor-1, warburg
Abstract: Now, at the beginning of a new century, 80 years after Warburgs Nobel prize winning discoveries, we are beginning to make sense of the underlying causes of the well known metabolic phenotype of tumor cells. Building on decades of research to understand the interrelationships between respiration and glycolysis in cancer, the tumor metabolic phenotype can now begin to be understood in a genomic context. With the discovery of hypoxia inducible factor-1 (HIF-1), which is widely overexpressed across a broad range of cancers, modern molecular tools have allowed us to put together the pattern of events that might explain the metabolic differences between tumor and normal cells. HIF-1 controls cellular and systemic responses to oxygen availability and coordinates upregulation of genes involved in many pathways concerned with tumour growth and metabolism including angiogenesis, glucose and energy metabolism, cellular proliferation, differentiation and viability, apoptosis, pH regulation and matrix metabolism. These findings begin to explain how glucose uptake and glycolysis could be up-regulated in cancer cells (through binding to a core DNA recognition sequence) in a co-ordinated and constitutive fashion that may also allow us to elucidate new targets for tumor therapy.
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Cite this article as:
Stubbs M., Bashford L. C. and Griffiths R. J., Understanding the Tumor Metabolic Phenotype in the Genomic Era, Current Molecular Medicine 2003; 3 (1) . https://dx.doi.org/10.2174/1566524033361645
DOI https://dx.doi.org/10.2174/1566524033361645 |
Print ISSN 1566-5240 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5666 |
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