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  Warburg effect and translocation-induced genomic instability: two yeast models for cancer cells

Tosato, V., Grüning, N.-M., Breitenbach, M., Arnak, R., Ralser, M., & Bruschi, C. V. (2013). Warburg effect and translocation-induced genomic instability: two yeast models for cancer cells. Frontiers in Oncology, 2: 212. doi:10.3389/fonc.2012.00212.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-000E-F0AB-B Version Permalink: http://hdl.handle.net/11858/00-001M-0000-000E-F0AC-9
Genre: Journal Article

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© 2013 Tosato, Grüning, Breitenbach, Arnak, Ralser and Bruschi. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in other forums, provided the original authors and source are credited and subject to any copyright notices concerning any third-party graphics etc.
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Tosato, V., Author
Grüning, N.-M.1, Author              
Breitenbach, M., Author
Arnak, R., Author
Ralser, M.1, Author              
Bruschi, C. V., Author
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1Dept. of Vertebrate Genomics (Head: Hans Lehrach), Max Planck Institute for Molecular Genetics, Max Planck Society, Berlin, Germany, ou_1433550              

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 Abstract: Yeast has been established as an efficient model system to study biological principles underpinning human health. In this review we focus on yeast models covering two aspects of cancer formation and progression (i) the activity of pyruvate kinase (PK), which recapitulates metabolic features of cancer cells, including the Warburg effect, and (ii) chromosome bridge-induced translocation (BIT) mimiking genome instability in cancer. Saccharomyces cerevisiae is an excellent model to study cancer cell metabolism, as exponentially growing yeast cells exhibit many metabolic similarities with rapidly proliferating cancer cells. The metabolic reconfiguration includes an increase in glucose uptake and fermentation, at the expense of respiration and oxidative phosphorylation (the Warburg effect), and involves a broad reconfiguration of nucleotide and amino acid metabolism. Both in yeast and humans, the regulation of this process seems to have a central player, PK, which is up-regulated in cancer, and to occur mostly on a post-transcriptional and post-translational basis. Furthermore, BIT allows to generate selectable translocation-derived recombinants ("translocants"), between any two desired chromosomal locations, in wild-type yeast strains transformed with a linear DNA cassette carrying a selectable marker flanked by two DNA sequences homologous to different chromosomes. Using the BIT system, targeted non-reciprocal translocations in mitosis are easily inducible. An extensive collection of different yeast translocants exhibiting genome instability and aberrant phenotypes similar to cancer cells has been produced and subjected to analysis. In this review, we hence provide an overview upon two yeast cancer models, and extrapolate general principles for mimicking human disease mechanisms in yeast.

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Language(s): eng - English
 Dates: 2013-01-18
 Publication Status: Published in print
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 Rev. Method: Peer
 Identifiers: DOI: 10.3389/fonc.2012.00212
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Title: Frontiers in Oncology
Source Genre: Journal
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Publ. Info: Frontiers Media S.A.
Pages: - Volume / Issue: 2 Sequence Number: 212 Start / End Page: - Identifier: -