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Published online July 2, 2007
doi:10.1083/jcb.200703099
The Journal of Cell Biology, Vol. 178, No. 1, 93-105
The Rockefeller University Press, 0021-9525 $30.00
© 2007 Yuneva et al.
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Article

 Deficiency in glutamine but not glucose induces MYC-dependent apoptosis in human cells

Mariia Yuneva1,2, Nicola Zamboni3, Peter Oefner4, Ravi Sachidanandam1, and Yuri Lazebnik1

1 Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724
2 G.W. Hooper Research Foundation, University of California at San Francisco, San Francisco, CA 94143
3 Institute of Molecular System Biology, ETH Zurich, 8093 Zurich, Switzerland
4 Institute of Functional Genomics, University of Regensburg, 93053 Regensburg, Germany

Correspondence to Yuri Lazebnik: lazebnik{at}cshl.edu

The idea that conversion of glucose to ATP is an attractive target for cancer therapy has been supported in part by the observation that glucose deprivation induces apoptosis in rodent cells transduced with the proto-oncogene MYC, but not in the parental line. Here, we found that depletion of glucose killed normal human cells irrespective of induced MYC activity and by a mechanism different from apoptosis. However, depletion of glutamine, another major nutrient consumed by cancer cells, induced apoptosis depending on MYC activity. This apoptosis was preceded by depletion of the Krebs cycle intermediates, was prevented by two Krebs cycle substrates, but was unrelated to ATP synthesis or several other reported consequences of glutamine starvation. Our results suggest that the fate of normal human cells should be considered in evaluating nutrient deprivation as a strategy for cancer therapy, and that understanding how glutamine metabolism is linked to cell viability might provide new approaches for treatment of cancer.

Abbreviations used in this paper: OHT, 4-hydroxytamoxifen; ROS, reactive oxygen species.


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