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Wnt/Snail signaling regulates cytochrome C oxidase and glucose metabolism

Su Yeon Lee1, Hyun Min Jeon, Min Kyung Ju

  • 1Department of Molecular Biology, College of Natural Sciences, Pusan National University, Pusan, Korea.

Cancer Research
|May 29, 2012
PubMed

Insights

Wnt signaling suppresses mitochondrial respiration and promotes glycolysis in cancer by regulating key enzyme expression. This pathway

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cancer Research

Background:

  • Wnt signaling is crucial in development and cancer, promoting tumor invasion and metastasis via epithelial-to-mesenchymal transition (EMT).
  • Deregulation of Wnt signaling is implicated in various cancers, including breast and colon cancer.

Purpose of the Study:

  • To investigate the role of Wnt signaling in regulating mitochondrial respiration and glucose metabolism in cancer.
  • To elucidate the molecular mechanisms underlying Wnt-mediated metabolic reprogramming.

Main Methods:

  • Studied the effect of Wnt signaling on mitochondrial respiration and cytochrome C oxidase (COX) activity.
  • Analyzed gene expression of COX subunits and pyruvate carboxylase (PC).
  • Investigated the involvement of the canonical β-catenin/T-cell factor 4/Snail pathway and EMT in metabolic regulation.

Main Results:

  • Wnt signaling suppresses mitochondrial respiration and COX activity by inhibiting COX subunit expression (COXVIc, COXVIIa, COXVIIc).
  • Wnt induces a metabolic switch to glycolysis, increasing glucose consumption and lactate production, and upregulating pyruvate carboxylase (PC).
  • EMT, induced by E-cadherin knockdown, mimics Wnt's effects on mitochondrial respiration and glycolysis, suggesting a link between EMT and Wnt/Snail-mediated metabolic control.

Conclusions:

  • Wnt/Snail signaling plays a novel role in regulating mitochondrial respiration via COX gene expression and glucose metabolism via PC gene expression.
  • These metabolic alterations are critical for tumor growth and progression.
  • EMT may contribute to Wnt/Snail's regulation of mitochondrial respiration and glucose metabolism.

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