Nature Communications (May 2017)
The distinct metabolic phenotype of lung squamous cell carcinoma defines selective vulnerability to glycolytic inhibition
- Justin Goodwin,
- Michael L. Neugent,
- Shin Yup Lee,
- Joshua H. Choe,
- Hyunsung Choi,
- Dana M. R. Jenkins,
- Robin J. Ruthenborg,
- Maddox W. Robinson,
- Ji Yun Jeong,
- Masaki Wake,
- Hajime Abe,
- Norihiko Takeda,
- Hiroko Endo,
- Masahiro Inoue,
- Zhenyu Xuan,
- Hyuntae Yoo,
- Min Chen,
- Jung-Mo Ahn,
- John D. Minna,
- Kristi L. Helke,
- Pankaj K. Singh,
- David B. Shackelford,
- Jung-whan Kim
Affiliations
- Justin Goodwin
- Department of Biological Sciences, The University of Texas at Dallas
- Michael L. Neugent
- Department of Biological Sciences, The University of Texas at Dallas
- Shin Yup Lee
- Department of Biological Sciences, The University of Texas at Dallas
- Joshua H. Choe
- Department of Biological Sciences, The University of Texas at Dallas
- Hyunsung Choi
- Department of Biological Sciences, The University of Texas at Dallas
- Dana M. R. Jenkins
- Department of Biological Sciences, The University of Texas at Dallas
- Robin J. Ruthenborg
- Department of Biological Sciences, The University of Texas at Dallas
- Maddox W. Robinson
- Department of Biological Sciences, The University of Texas at Dallas
- Ji Yun Jeong
- Department of Pathology, School of Medicine, Kyungpook National University
- Masaki Wake
- Department of Cardiovascular Medicine, The University of Tokyo
- Hajime Abe
- Department of Cardiovascular Medicine, The University of Tokyo
- Norihiko Takeda
- Department of Cardiovascular Medicine, The University of Tokyo
- Hiroko Endo
- Department of Biochemistry, Osaka International Cancer Institute
- Masahiro Inoue
- Department of Biochemistry, Osaka International Cancer Institute
- Zhenyu Xuan
- Department of Biological Sciences, The University of Texas at Dallas
- Hyuntae Yoo
- Department of Biological Sciences, The University of Texas at Dallas
- Min Chen
- Department of Mathematical Sciences, The University of Texas at Dallas
- Jung-Mo Ahn
- Department of Chemistry and Biochemistry, The University of Texas at Dallas
- John D. Minna
- Department of Medicine and Pharmacology, Hamon Center for Therapeutic Oncology Research, Simmons Comprehensive Cancer Center, The University of Texas Southwestern Medical Center
- Kristi L. Helke
- Pankaj K. Singh
- Department of Biochemistry and Molecular Biology, Department of Genetics, Department of Pathology and Microbiology, The Eppley Institute for Cancer and Allied Diseases, Cell Biology and Anatomy, University of Nebraska Medical Center
- David B. Shackelford
- Department of Pulmonary and Critical Care Medicine, David Geffen, School of Medicine, University of California
- Jung-whan Kim
- Department of Biological Sciences, The University of Texas at Dallas
- DOI
- https://doi.org/10.1038/ncomms15503
- Journal volume & issue
-
Vol. 8,
no. 1
pp. 1 – 16
Abstract
Adenocarcinoma and squamous cell carcinoma are distinct subtypes of non-small cell lung cancer. Here, the authors show that increased glycolytic flux, via increased glucose transporter Glut1 expression, is a core metabolic feature of squamous cell carcinoma that renders it sensitive to glycolysis inhibition.
