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Environment Impacts the Metabolic Dependencies of Ras-Driven Non-Small Cell Lung Cancer.
Davidson, Shawn M; Papagiannakopoulos, Thales; Olenchock, Benjamin A; Heyman, Julia E; Keibler, Mark A; Luengo, Alba; Bauer, Matthew R; Jha, Abhishek K; O'Brien, James P; Pierce, Kerry A; Gui, Dan Y; Sullivan, Lucas B; Wasylenko, Thomas M; Subbaraj, Lakshmipriya; Chin, Christopher R; Stephanopolous, Gregory; Mott, Bryan T; Jacks, Tyler; Clish, Clary B; Vander Heiden, Matthew G.
Afiliación
  • Davidson SM; Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02142, USA; Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA; Broad Institute of MIT and Harvard University, Cambridge, MA 02142, USA.
  • Papagiannakopoulos T; Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.
  • Olenchock BA; Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02142, USA; Broad Institute of MIT and Harvard University, Cambridge, MA 02142, USA; Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA.
  • Heyman JE; Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.
  • Keibler MA; Department of Chemical Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
  • Luengo A; Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02142, USA; Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
  • Bauer MR; Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.
  • Jha AK; Elucidata Corporation, Cambridge, MA 02139, USA.
  • O'Brien JP; Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.
  • Pierce KA; Broad Institute of MIT and Harvard University, Cambridge, MA 02142, USA.
  • Gui DY; Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.
  • Sullivan LB; Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.
  • Wasylenko TM; Department of Chemical Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
  • Subbaraj L; Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.
  • Chin CR; Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.
  • Stephanopolous G; Department of Chemical Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
  • Mott BT; National Center for Advancing Translational Sciences, NIH, Bethesda, MD 20892, USA.
  • Jacks T; Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02142, USA; Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
  • Clish CB; Broad Institute of MIT and Harvard University, Cambridge, MA 02142, USA.
  • Vander Heiden MG; Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02142, USA; Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA; Broad Institute of MIT and Harvard University, Cambridge, MA 02142, USA; Dana-Farber Cancer Institu
Cell Metab ; 23(3): 517-28, 2016 Mar 08.
Article en En | MEDLINE | ID: mdl-26853747
Cultured cells convert glucose to lactate, and glutamine is the major source of tricarboxylic acid (TCA)-cycle carbon, but whether the same metabolic phenotype is found in tumors is less studied. We infused mice with lung cancers with isotope-labeled glucose or glutamine and compared the fate of these nutrients in tumor and normal tissue. As expected, lung tumors exhibit increased lactate production from glucose. However, glutamine utilization by both lung tumors and normal lung was minimal, with lung tumors showing increased glucose contribution to the TCA cycle relative to normal lung tissue. Deletion of enzymes involved in glucose oxidation demonstrates that glucose carbon contribution to the TCA cycle is required for tumor formation. These data suggest that understanding nutrient utilization by tumors can predict metabolic dependencies of cancers in vivo. Furthermore, these data argue that the in vivo environment is an important determinant of the metabolic phenotype of cancer cells.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Carcinoma de Pulmón de Células no Pequeñas / Microambiente Tumoral / Neoplasias Pulmonares Límite: Animals / Humans Idioma: En Revista: Cell Metab Asunto de la revista: METABOLISMO Año: 2016 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Carcinoma de Pulmón de Células no Pequeñas / Microambiente Tumoral / Neoplasias Pulmonares Límite: Animals / Humans Idioma: En Revista: Cell Metab Asunto de la revista: METABOLISMO Año: 2016 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos