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Updated: Aug 23, 2025

Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes
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Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes

Published on: January 7, 2013

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PRL stimulates mitotic errors by suppressing kinetochore-localized activation of AMPK during mitosis

Kajung Ryu1, Atsushi Yoshida1, Yosuke Funato1

  • 1Department of Cellular Regulation, Research Institute for Microbial Diseases, Osaka University.

Cell Structure and Function
|November 6, 2022
PubMed

Insights

Phosphatase of regenerating liver (PRL) overexpression drives cancer by causing mitotic errors. Activating AMP-activated protein kinase (AMPK) corrects these errors, highlighting AMPK

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • Phosphatase of regenerating liver (PRL) is overexpressed in many cancers, promoting malignancy.
  • Mitotic errors, including spindle misorientation and aneuploidy, are hallmarks of cancer progression.

Purpose of the Study:

  • To investigate the role of PRL in mitotic errors.
  • To elucidate the mechanistic link between PRL and mitotic regulation.
  • To explore therapeutic potential of targeting AMPK in PRL-driven cancers.

Main Methods:

  • Immunofluorescence analysis to assess P-AMPK levels at kinetochores.
  • Utilizing chemical activators (A769662, AICAR) to activate AMPK.
  • Observing spindle orientation and aneuploidy in PRL-expressing cells.

Main Results:

  • PRL overexpression reduces phosphorylated AMPK (P-AMPK) at kinetochores, leading to mitotic errors.
  • Activation of AMPK by chemical activators restores P-AMPK at kinetochores.
  • AMPK activation normalizes spindle orientation and corrects mitotic errors in PRL-expressing cells.

Conclusions:

  • Kinetochore-localized AMPK activation is essential for accurate mitosis.
  • PRL overexpression disrupts mitosis by inhibiting AMPK activation.
  • Targeting AMPK represents a potential strategy to counteract PRL-driven cancer progression.
Keywords:
AMPKPRLcancerkinetochoremitotic errors

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