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Role of p90(RSK) in regulating the Crabtree effect: implications for cancer

Emily K Redman1, Paul S Brookes, Marcin K Karcz

  • 1School of Medicine, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642, USA.

Biochemical Society Transactions
|January 30, 2013
PubMed

Insights

High glucose impairs mitochondrial respiration, the Crabtree effect, in cancer cells. This study explores the role of p90 ribosomal S6 kinase (RSK) and ERK MAPKs in regulating this metabolic shift.

Area of Science:

  • Biochemistry
  • Cancer Biology
  • Metabolic Regulation

Background:

  • The Crabtree effect describes high glucose-induced inhibition of mitochondrial respiration in cancer cells.
  • Upstream regulators of the Crabtree effect, particularly in the context of elevated glucose like in diabetes, are not well understood.
  • p90 ribosomal S6 kinase (RSK) is implicated in high glucose effects and cancer signaling, but its role in cancer cell metabolism is unclear.

Purpose of the Study:

  • To provide an overview of the Crabtree effect and its connection to mitochondrial metabolism.
  • To investigate the potential role of p90 RSK and its upstream regulators, ERK MAPKs, in the Crabtree effect.
  • To clarify the involvement of p90 RSK in cancer cell metabolic regulation.

Main Methods:

  • Literature review on the Crabtree effect and mitochondrial metabolism.
  • Presentation of preliminary data investigating signaling pathways.
  • Analysis of the relationship between p90 RSK, ERK MAPKs, and the Crabtree effect.

Main Results:

  • Preliminary data suggest a role for p90 RSK in the Crabtree effect.
  • The upstream ERK (extracellular-signal-regulated kinase) family of MAPKs (mitogen-activated protein kinases) may also be involved.
  • This study highlights potential mediators of high glucose-induced metabolic changes in cancer cells.

Conclusions:

  • p90 RSK and ERK MAPKs are potentially key regulators of the Crabtree effect.
  • Further research is needed to fully elucidate the mechanisms linking these pathways to cancer cell metabolism.
  • Understanding these pathways could offer new therapeutic targets for metabolic dysregulation in cancer.

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