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Overexpression of tumor necrosis factor receptor-associated protein 1 (TRAP1), leads to mitochondrial aberrations in

Chang-Nim Im1, Jeong-Sun Seo2

  • 1Department of Biochemistry and Molecular Biology, Seoul National University College of Medicine; ILCHUN Molecular Medicine Institute MRC, Seoul 110-799; Department of Biochemistry, The Catholic University of Korea College of Medicine, Seoul 137-701, Korea.

BMB Reports
|November 30, 2013
PubMed

Insights

Overexpression of Tumor Necrosis Factor Receptor-Associated Protein 1 (TRAP1) in cells causes mitochondrial damage and increases proliferation. This suggests TRAP1 links mitochondrial dysfunction to cancer development.

Area of Science:

  • Mitochondrial biology
  • Cancer research
  • Cellular signaling

Background:

  • Cancer cells exhibit uncontrolled proliferation and abnormal mitochondria.
  • Tumor necrosis factor receptor-associated protein 1 (TRAP1), a mitochondrial heat shock protein, is highly expressed in some cancers.
  • The precise impact of TRAP1 overexpression on mitochondrial function remains largely unknown.

Purpose of the Study:

  • To investigate the mitochondrial alterations associated with TRAP1 overexpression.
  • To explore the relationship between TRAP1, mitochondrial function, and cellular proliferation in a mouse cell line.

Main Methods:

  • Utilized NIH/3T3 mouse cell line for experiments.
  • Assessed mitochondrial changes, reactive oxygen species (ROS) levels, and mitochondrial biogenesis.
  • Measured peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α) mRNA levels and extracellular signal-regulated kinase (ERK) phosphorylation.

Main Results:

  • TRAP1 overexpression led to increased basal ROS levels.
  • Observed a decrease in mitochondrial biogenesis and PGC-1α mRNA levels.
  • Noted increased ERK phosphorylation and enhanced proliferation in TRAP1-overexpressing cells.

Conclusions:

  • TRAP1 overexpression induces significant mitochondrial aberrations, including elevated ROS and reduced biogenesis.
  • The findings indicate a potential role for TRAP1 in linking mitochondrial disturbances to cancer progression.
  • TRAP1 may influence cellular proliferation through modulation of the ERK signaling pathway.

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