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Niclosamide induces mitochondria fragmentation and promotes both apoptotic and autophagic cell death

So Jung Park1, Ji Hyun Shin, Hee Kang

  • 1Graduate School of East-West Medical Science, Kyung Hee University, Yongin, Korea.

BMB Reports
|August 30, 2011
PubMed

Insights

Niclosamide triggers mitochondrial fragmentation, disrupting cell energy and promoting both apoptosis and autophagy. This suggests niclosamide

Area of Science:

  • Cell Biology
  • Biochemistry
  • Pharmacology

Background:

  • Mitochondrial dynamics encompass morphology, biogenesis, distribution, and cell death.
  • Identifying regulators of mitochondrial dynamics is crucial for understanding cellular processes.

Purpose of the Study:

  • To screen for chemical compounds that regulate mitochondrial dynamics.
  • To investigate the effects of niclosamide on mitochondrial function and cell death pathways.

Main Methods:

  • Chemical library screening to identify regulators of mitochondrial fission.
  • Down-regulation of dynamin-related protein 1 (Drp1) to assess its role.
  • Measurement of mitochondrial membrane potential and ATP levels.
  • Caspase-3 activation assays for apoptosis.
  • Assessment of autophagic activity.

Main Results:

  • Niclosamide was identified as a potent inducer of mitochondrial fission.
  • Niclosamide-induced fragmentation was dependent on Drp1.
  • Treatment decreased mitochondrial membrane potential and ATP levels.
  • Niclosamide induced apoptotic cell death via caspase-3 activation.
  • Niclosamide increased autophagic activity, which was essential for cell death.

Conclusions:

  • Niclosamide induces mitochondrial fragmentation.
  • Niclosamide contributes to cell death through both apoptosis and autophagy.
  • Drp1 is a key mediator of niclosamide's effects on mitochondrial dynamics.

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