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PARK2 loss promotes cancer progression via redox-mediated inactivation of PTEN

Amit Gupta1, Sara Anjomani-Virmouni1, Nikos Koundouros1,2

  • 1Signalling and Cancer Metabolism Team, Division of Cancer Biology, The Institute of Cancer Research, London, UK.

Molecular & Cellular Oncology
|December 7, 2017
PubMed

Insights

Loss of the Parkinson disease gene parkin (PARK2) promotes cancer. This occurs through redox-mediated inactivation of PTEN, a tumor suppressor, via S-nitrosylation, linking neurodegeneration and cancer pathways.

Area of Science:

  • Molecular biology
  • Neuroscience
  • Oncology

Background:

  • Parkinson disease (PD) and cancer involve distinct cellular alterations.
  • Pathogenic mutations can be linked to both PD and cancer.
  • The parkin gene (PRKN/PARK2) is genetically linked to PD.

Purpose of the Study:

  • To investigate the role of parkin loss in cancer progression.
  • To elucidate the mechanism by which parkin deficiency impacts tumor suppressor function.

Main Methods:

  • Analysis of redox-mediated inactivation pathways.
  • Investigation of S-nitrosylation of phosphatase and tensin homolog (PTEN).

Main Results:

  • Loss of parkin (PRKN/PARK2) promotes cancer progression.
  • Parkin deficiency leads to redox-mediated inactivation of PTEN.
  • PTEN inactivation occurs via S-nitrosylation.

Conclusions:

  • Parkin loss links Parkinson disease genetics to cancer promotion.
  • Redox-mediated PTEN inactivation is a key mechanism connecting PD and cancer.
  • Targeting S-nitrosylation pathways may offer therapeutic strategies for both diseases.
Keywords:
CancerPARK2PTENS-nitrosylationnitrosative stress

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