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Orphan nuclear receptor TR3 acts in autophagic cell death via mitochondrial signaling pathway

Wei-jia Wang1, Yuan Wang1, Hang-zi Chen1

  • 11] State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Biology, School of Life Sciences, Xiamen University, Xiamen, Fujian Province, China. [2].

Nature Chemical Biology
|December 10, 2013
PubMed

Insights

Melanoma cells can be induced to undergo autophagic cell death via a novel compound targeting the orphan nuclear receptor TR3. This process involves TR3

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • Autophagy's role in cell death is not fully understood.
  • Melanoma is typically resistant to apoptosis.
  • Orphan nuclear receptor TR3's function in cell death requires further elucidation.

Purpose of the Study:

  • To investigate the mechanisms of autophagic cell death in melanoma.
  • To identify compounds that can induce cell death in drug-resistant melanoma.
  • To explore the role of TR3 in melanoma cell demise.

Main Methods:

  • Screening of TR3-targeting compounds.
  • Investigating molecular events leading to cell death.
  • Analyzing TR3 translocation to mitochondria and its interactions with mitochondrial proteins (Nix, Tom40, Tom70).
  • Assessing mitochondrial membrane potential dissipation and autophagy induction.

Main Results:

  • A novel compound, 1-(3,4,5-trihydroxyphenyl)nonan-1-one, induces autophagic cell death in melanoma.
  • TR3 plays a crucial role in this process.
  • The cascade involves TR3 translocation to mitochondria, mitochondrial membrane potential dissipation, and subsequent autophagy.
  • Excessive mitochondria clearance leads to irreversible cell death.

Conclusions:

  • Melanoma can undergo autophagic cell death mediated by TR3.
  • A specific chemical compound activates a mitochondrial signaling pathway involving TR3 and autophagy.
  • This pathway offers a potential new therapeutic strategy for melanoma treatment.

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