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PRAME/EZH2-mediated regulation of TRAIL: a new target for cancer therapy

D D De Carvalho1, B P Mello, W O Pereira

  • 1Ontario Cancer Institute, Princess Margaret Hospital, University Health Network, Toronto, Canada. ddecarv@uhnres.utoronto.ca

Current Molecular Medicine
|December 12, 2012
PubMed

Insights

Restoring tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) expression by inhibiting repressors like PRAME/EZH2 offers a novel cancer therapy strategy. This approach aims to induce tumor-selective cell death, overcoming limitations of existing TRAIL-based treatments.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Therapeutics

Background:

  • The tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) pathway is a promising target for cancer therapy due to its cancer cell-specific pro-apoptotic activity.
  • Current therapeutic strategies utilizing TRAIL, including recombinant TRAIL, agonist antibodies, and adenoviral TRAIL, face limitations in clinical application.

Purpose of the Study:

  • To investigate the role of the PRAME/EZH2 complex in repressing TRAIL expression in cancer cells.
  • To propose a novel therapeutic strategy based on inhibiting TRAIL repressors to restore endogenous TRAIL expression for combined cancer therapy.

Main Methods:

  • The study focuses on the discovery of the PRAME/EZH2 complex's function in repressing TRAIL expression.
  • The proposed approach involves genetic or pharmacological inhibition of TRAIL repressors within cancer cells.

Main Results:

  • The PRAME/EZH2 complex was identified as a repressor of TRAIL expression in a cancer-specific manner.
  • Inhibition of TRAIL repressors is suggested to restore endogenous TRAIL expression in cancer cells.

Conclusions:

  • Targeting TRAIL repressors like PRAME/EZH2 presents an alternative and potentially synergistic approach for cancer therapy.
  • This strategy may overcome limitations of current TRAIL-based therapies and enhance tumor-selective cell death.

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