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PRR5, a novel component of mTOR complex 2, regulates platelet-derived growth factor receptor beta expression and

So-Yon Woo1, Dong-Hwan Kim, Chang-Bong Jun

  • 1Department of Biochemistry, Molecular Biology, and Biophysics, University of Minnesota at the Twin Cities, Minneapolis, Minnesota 55455, USA.

The Journal of Biological Chemistry
|June 30, 2007
PubMed

Insights

Researchers identified PRR5, a new mTORC2 component, impacting cell growth and tumorigenesis. PRR5 silencing inhibits Akt and S6K1 phosphorylation, affecting PDGFRbeta signaling and cell proliferation.

Area of Science:

  • Cellular Biology
  • Molecular Biology
  • Biochemistry

Background:

  • The mammalian target of rapamycin (mTOR) pathway regulates cellular responses to nutrients and growth factors.
  • mTOR forms two complexes, mTORC1 and mTORC2, with distinct functions.
  • mTORC2's roles are less understood compared to mTORC1.

Purpose of the Study:

  • Identify novel components of mTORC2.
  • Investigate the function of a newly identified mTORC2 component, PRR5.
  • Elucidate PRR5's role in cell signaling, proliferation, and tumorigenesis.

Main Methods:

  • Protein-protein interaction studies to identify PRR5 binding partners.
  • Gene silencing (knockdown) of PRR5 to assess its functional impact.
  • Western blotting to measure protein phosphorylation (Akt, S6K1).
  • Cell proliferation assays.
  • Analysis of platelet-derived growth factor receptor beta (PDGFRbeta) expression.

Main Results:

  • PRR5 interacts with rictor, a component of mTORC2.
  • PRR5 is not essential for mTORC2-mediated Akt phosphorylation.
  • PRR5 silencing inhibits Akt and S6K1 phosphorylation and reduces cell proliferation.
  • PRR5 knockdown correlates with reduced PDGFRbeta expression.
  • PRR5 silencing impairs PDGF-stimulated Akt and S6K1 phosphorylation.

Conclusions:

  • PRR5 is a novel component of mTORC2 with implications in cell growth and tumorigenesis.
  • PRR5 plays a role in regulating Akt and S6K1 phosphorylation, potentially through PDGFRbeta signaling.
  • mTORC2 may crosstalk with pathways regulating PDGFRbeta expression and signaling.

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