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Oncogenic K-Ras decouples glucose and glutamine metabolism to support cancer cell growth

Daniela Gaglio1, Christian M Metallo, Paulo A Gameiro

  • 1Department of Biotechnology and Biosciences, University of Milano-Bicocca, Milan, Italy.

Molecular Systems Biology
|August 18, 2011
PubMed

Insights

Oncogenic K-Ras reprograms cancer cell metabolism, enhancing glycolysis and glutamine use while decreasing TCA cycle flux. This metabolic shift fuels tumor growth and biosynthesis.

Area of Science:

  • Oncology
  • Metabolic Engineering
  • Cancer Biology

Background:

  • Oncogenes, like K-ras, drive cellular transformation and tumorigenesis.
  • Cancer cells exhibit altered metabolism to support rapid proliferation.
  • Understanding oncogene-driven metabolic changes is crucial for cancer therapy.

Purpose of the Study:

  • To investigate the metabolic alterations induced by oncogenic K-Ras.
  • To elucidate the role of K-Ras in regulating central carbon metabolism.
  • To identify key metabolic pathways affected during K-Ras-mediated transformation.

Main Methods:

  • Utilized ¹³C metabolic flux analysis (MFA) and ¹⁵N-labeled glutamine tracing.
  • Employed non-targeted tracer fate detection (NTFD) and transcriptomic profiling.
  • Analyzed metabolic fluxes in mouse fibroblast and human carcinoma cell lines.

Main Results:

  • Oncogenic K-Ras-expressing cells showed increased glycolysis and glutamine utilization for anabolism.
  • A decreased oxidative flux through the tricarboxylic acid (TCA) cycle was observed.
  • Transcriptomic data revealed elevated expression of genes in glycolysis, glutamine metabolism, and nucleotide biosynthesis pathways.

Conclusions:

  • Oncogenic K-Ras significantly reprograms cancer cell metabolism, decoupling glycolysis from the TCA cycle.
  • Glutamine serves as a critical carbon source to support anabolic processes in K-Ras-transformed cells.
  • These findings highlight K-Ras's role in metabolic reprogramming essential for cancer cell survival and growth.

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