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  BCAT1 promotes cell proliferation through amino acid catabolism in gliomas carrying wild-type IDH1

Tönjes, M., Barbus, S., Park, Y. J., Wang, W., Schlotter, M., Lindroth, A. M., et al. (2013). BCAT1 promotes cell proliferation through amino acid catabolism in gliomas carrying wild-type IDH1. Nature Medicine, 19(7): 1, pp. 901-908. doi:10.1038/nm.3217.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-0014-C5FD-3 Version Permalink: http://hdl.handle.net/11858/00-001M-0000-002E-7D6C-5
Genre: Journal Article

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 Creators:
Tönjes, Martje, Author
Barbus, Sebastian, Author
Park, Yoon Jung, Author
Wang, Wei, Author
Schlotter, Magdalena, Author
Lindroth, Anders M., Author
Pleier, Sabrina V., Author
Bai, Alfa H.C., Author
Karra, Daniela, Author
Piro, Rosario M., Author
Felsberg, Jörg, Author
Addington, Adele, Author
Lemke, Dieter, Author
Weibrecht, Irene, Author
Hovestadt, Volker, Author
Rolli, Claudio G., Author              
Campos, Benito, Author
Turcan, Sevin, Author
Sturm, Dominik, Author
Witt, Hendrik, Author
Chan, Timothy A., AuthorHerold-Mende, Christel, AuthorKemkemer, Ralf1, Author              König, Rainer, AuthorSchmidt, Kathrin, AuthorHull, William-Edmund, AuthorPfister, Stefan M., AuthorJugold, Manfred, AuthorHutson, Susan M., AuthorPlass, Christoph, AuthorOkun, Jürgen G., AuthorReifenberger, Guido, AuthorLichter, Peter, AuthorRadlwimmer, Bernhard, Author more..
Affiliations:
1Cellular Biophysics, Max Planck Institute for Medical Research, Max Planck Society, ou_2364731              

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 Abstract: Here we show that glioblastoma express high levels of branched-chain amino acid transaminase 1 (BCAT1), the enzyme that initiates the catabolism of branched-chain amino acids (BCAAs). Expression of BCAT1 was exclusive to tumors carrying wild-type isocitrate dehydrogenase 1 (IDH1) and IDH2 genes and was highly correlated with methylation patterns in the BCAT1 promoter region. BCAT1 expression was dependent on the concentration of α-ketoglutarate substrate in glioma cell lines and could be suppressed by ectopic overexpression of mutant IDH1 in immortalized human astrocytes, providing a link between IDH1 function and BCAT1 expression. Suppression of BCAT1 in glioma cell lines blocked the excretion of glutamate and led to reduced proliferation and invasiveness in vitro, as well as significant decreases in tumor growth in a glioblastoma xenograft model. These findings suggest a central role for BCAT1 in glioma pathogenesis, making BCAT1 and BCAA metabolism attractive targets for the development of targeted therapeutic approaches to treat patients with glioblastoma.

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Language(s): eng - English
 Dates: 2013-02-152013-05-012013-06-232013-07-01
 Publication Status: Published in print
 Pages: 8
 Publishing info: -
 Table of Contents: -
 Rev. Type: Peer
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Title: Nature Medicine
  Other : Nat. Med.
Source Genre: Journal
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Publ. Info: New York, NY : Nature Pub. Co.
Pages: - Volume / Issue: 19 (7) Sequence Number: 1 Start / End Page: 901 - 908 Identifier: ISSN: 1078-8956
CoNE: https://pure.mpg.de/cone/journals/resource/954925606824