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Epigenetic Marks Repressing Gluconeogenesis in Liver and Kidney Cancer

Katharina Leithner1

  • 1Division of Pulmonology, Department of Internal Medicine, Medical University of Graz, Graz, Austria. katharina.leithner@medunigraz.at.

Cancer Research
|February 16, 2020
PubMed

Insights

Researchers found that Polycomb Repressive Complex 2 (PRC2) downregulates fructose-1,6-bisphosphatase (FBP1) in liver and kidney cancers. This repression is a key mechanism in cancer development, disrupting a crucial feedback loop.

Area of Science:

  • Cancer Biology
  • Epigenetics
  • Metabolic Regulation

Background:

  • Gluconeogenesis is often suppressed in tumors from gluconeogenic organs.
  • Re-expression of fructose-1,6-bisphosphatase (FBP1) inhibits tumor growth.

Purpose of the Study:

  • To investigate the mechanism of FBP1 downregulation in cancer.
  • To identify the role of FBP1 repression in Polycomb Repressive Complex 2 (PRC2)-mediated carcinogenesis.

Main Methods:

  • Analysis of histone modifications, specifically H3K27 trimethylation.
  • Assessment of FBP1 expression in liver and kidney cancer cells.
  • Investigation of the interaction between FBP1 and PRC2.

Main Results:

  • PRC2 induces histone H3 trimethylation on lysine 27 (H3K27me3), leading to FBP1 downregulation in liver and kidney cancer cells.
  • FBP1 repression is identified as a downstream effect of PRC2 in carcinogenesis.
  • FBP1 was found to inhibit glycolysis and directly interfere with PRC2 function.

Conclusions:

  • FBP1 and PRC2 form a novel negative feedback loop that is disrupted in liver and kidney cancer.
  • PRC2-mediated FBP1 repression is a significant mechanism in cancer development.
  • Targeting this feedback loop may offer therapeutic strategies for liver and kidney cancers.

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