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Axin1 expression facilitates cell death induced by aurora kinase inhibition through PARP activation

Eun-Jin Choi1, Shi-Mun Kim, Ki-Joon Song

  • 1Laboratory of Cell Biology, Department of Microbiology and Bank for Pathogenic Virus, College of Medicine, Korea University, Seoul 136-705, Korea.

Journal of Cellular Biochemistry
|April 27, 2011
PubMed

Insights

Axin1 expression sensitizes cells to Aurora kinase inhibition, causing cell death via poly(ADP-ribose) polymerase (PARP) and apoptosis-inducing factor (AIF) pathways. Axin2-expressing cells, however, survived this inhibition.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Axin proteins are negative regulators of Wnt signaling.
  • Axin1 localizes to centrosomes and mitotic spindles, requiring Aurora kinase activity.
  • Aurora kinase activity influences cell division and apoptosis.

Purpose of the Study:

  • To investigate the role of Axin1 and Axin2 in cellular response to Aurora kinase inhibition.
  • To elucidate the mechanisms of cell death induced by Aurora kinase inhibition in Axin1-expressing cells.

Main Methods:

  • Cell culture of L-Axin and L-Axin2 expressing cells.
  • Treatment with Aurora kinase inhibitor (AKI).
  • Analysis of cell death markers, poly(ADP-ribose) polymerase (PARP) activation, ATP levels, mitochondrial apoptosis-inducing factor (AIF) release, and caspase-3 activation.
  • Gene knockdown of AIF.

Main Results:

  • Aurora inhibition of Axin1-expressing cells (L-Axin) induced polyploidy and cell death with apoptotic signs.
  • Axin2-expressing cells (L-Axin2) survived Aurora inhibition.
  • AKI treatment activated PARP, reduced ATP, and induced AIF release in L-Axin cells.
  • PARP inhibition and AIF knockdown partially reduced AKI-induced cell death.

Conclusions:

  • Axin1 expression confers sensitivity to Aurora inhibition-induced cell death.
  • This cell death is dependent on poly(ADP-ribose) polymerase (PARP) activation and apoptosis-inducing factor (AIF) release.
  • Axin2 does not confer sensitivity to Aurora inhibition-induced cell death.

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