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TRADD is critical for resistance to TRAIL-induced cell death through NF-κB activation

Joo-Young Kim1, Ju-Yeon Lee, Dong-Gun Kim

  • 1Institute for Medical Sciences, Ajou University School of Medicine, Suwon, Republic of Korea.

FEBS Letters
|June 2, 2011
PubMed

Insights

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) resistance is a major hurdle in cancer therapy. TRADD deficiency sensitizes cancer cells to TRAIL, suggesting TRADD as a potential therapeutic target to overcome resistance.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Immunology

Background:

  • Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a promising cancer therapeutic agent.
  • Acquisition of TRAIL resistance is a significant obstacle to its clinical efficacy.

Purpose of the Study:

  • To investigate the role of TRADD (TRAF-associated death domain) in TRAIL-induced apoptosis.
  • To determine if TRADD is involved in TRAIL resistance mechanisms.

Main Methods:

  • Utilized TRADD-deficient mouse embryonic fibroblasts (MEFs).
  • Employed siRNA-mediated knockdown of TRADD in cancer cell lines.
  • Assessed TRAIL-induced apoptosis and NF-κB activation.

Main Results:

  • TRADD deficiency significantly sensitized cells to TRAIL-induced apoptosis.
  • Enhanced cell death in TRADD(-/-) MEFs correlated with defective NF-κB activation.
  • siRNA knockdown of TRADD in cancer cells also increased sensitivity to TRAIL.

Conclusions:

  • TRADD plays a pro-survival role in TRAIL signaling, at least partially through NF-κB activation.
  • Targeting TRADD may represent a viable strategy to overcome TRAIL resistance in cancer therapy.

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