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Published on: July 21, 2018

Proliferation-independent control of tumor glycolysis by PDGFR-mediated AKT activation

Cong Ran1, Huan Liu, Yasuyuki Hitoshi

  • 1Department of Pediatrics and Genetics, Norris Cotton Cancer Center, Hanover, New Hampshire, USA.

Cancer Research
|January 17, 2013
PubMed

Insights

Platelet-derived growth factor (PDGF) signaling directly regulates glycolysis in glioma cells, independent of cell proliferation. This pathway requires AKT activation, offering potential therapeutic targets for brain tumors by inhibiting energy metabolism.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Tumor cells exhibit altered glucose metabolism, a hallmark of cancer.
  • Receptor tyrosine kinase (RTK) pathways influence tumor proliferation and energy metabolism.
  • Previous studies linked RTK-driven proliferation to altered glycolysis, obscuring direct glycolytic regulation.

Purpose of the Study:

  • To investigate if RTKs regulate glycolysis independently of cell proliferation.
  • To identify specific RTK pathways controlling glycolysis in brain tumors.

Main Methods:

  • Utilized a novel mouse model of glioma-derived tumor stem-like cells.
  • Investigated the platelet-derived growth factor (PDGF)/PDGF receptor (PDGFR) signaling pathway.
  • Assessed the role of AKT activation in PDGF-mediated glycolysis.

Main Results:

  • Identified PDGF/PDGFR signaling as a regulator of glycolysis in glioma stem-like cells.
  • Demonstrated that PDGF-regulated glycolysis is independent of PDGF-regulated proliferation.
  • Confirmed that AKT activation is essential for PDGF-induced glycolysis.

Conclusions:

  • RTKs can directly regulate tumor glycolysis without altering proliferation.
  • The PDGF/PDGFR/AKT pathway is a key regulator of aerobic glycolysis in brain tumors.
  • Targeting this pathway offers a strategy to inhibit tumor energy metabolism and treat brain tumors.

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