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Updated: Mar 23, 2026

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CK2 inhibition induced PDK4-AMPK axis regulates metabolic adaptation and survival responses in glioma

Deobrat Dixit1, Fahim Ahmad1, Ruchi Ghildiyal1

  • 1National Brain Research Centre, Manesar, Haryana, India.

Experimental Cell Research
|March 23, 2016
PubMed

Insights

Inhibiting Casein Kinase 2 (CK2) in glioma cells disrupts glucose metabolism via the PDK4-AMPK pathway, hindering cancer cell survival and tumor growth. This metabolic reprogramming offers a promising therapeutic strategy for aggressive brain tumors.

Area of Science:

  • Molecular Biology
  • Cancer Metabolism
  • Neuro-oncology

Background:

  • Aberrant metabolic adaptation and pro-survival mechanisms in glioma cells are critical therapeutic targets.
  • Casein Kinase 2 (CK2) has been previously linked to glioma cell survival.

Purpose of the Study:

  • To investigate the role of CK2 in regulating glucose metabolism in glioma cells.
  • To elucidate the molecular mechanisms linking CK2 inhibition to metabolic changes and cell survival.

Main Methods:

  • Inhibition of CK2 using 4,5,6,7-Tetrabromobenzotriazole (TBB) in vitro and in vivo.
  • Analysis of metabolic regulators (PDK4, AMPK, CREB) expression and phosphorylation.
  • Assessment of glucose uptake and cell viability.
  • Evaluation of tumor growth in athymic nude mouse xenograft models.

Main Results:

  • CK2 inhibition increased PDK4 and AMPK expression, leading to decreased glucose uptake in a PDK4/AMPK-dependent manner.
  • PDK4 upregulation was dependent on the cellular energy sensor CREB.
  • PDK4 regulated AMPK phosphorylation, impacting glioma cell viability.
  • TBB treatment significantly retarded glioma xenograft growth, with increased senescence, pAMPK, and PDK4 levels in tumors.

Conclusions:

  • CK2 inhibition modulates the PDK4-AMPK signaling axis, altering metabolic profiles and impacting glioma cell survival.
  • Targeting CK2 represents a potential therapeutic strategy for glioma by disrupting cancer cell metabolism.
Keywords:
AMPKCK2CREBGlioblastomaPDK4

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