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Mcl-1: a gateway to TRAIL sensitization

Seok-Hyun Kim1, M Stacey Ricci, Wafik S El-Deiry

  • 1Laboratory of Molecular Oncology and Cell Cycle Regulation, Department of Medicine, Institute for Translational Medicine and Therapeutics, Abramson Comprehensive Cancer Center, University of Pennsylvania School of Medicine, Philadelphia, PA, USA.

Cancer Research
|April 3, 2008
PubMed

Insights

Combining tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) with sorafenib enhances cancer cell killing. This combination therapy, by down-regulating Mcl-1, offers a promising strategy against difficult-to-treat cancers.

Area of Science:

  • Oncology
  • Molecular Biology
  • Drug Development

Background:

  • The proapoptotic cytokine tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) shows potential as a selective anticancer agent.
  • Limited efficacy of TRAIL against certain cancer cell lines raises concerns about its clinical utility.

Purpose of the Study:

  • To review findings on enhancing cancer cell sensitivity to TRAIL.
  • To explore the role of Mcl-1 down-regulation in TRAIL-mediated apoptosis.

Main Methods:

  • Review of recent scientific literature.
  • Analysis of the effects of sorafenib on Mcl-1 expression.
  • Investigation of combination therapy strategies.

Main Results:

  • Sorafenib, a Raf/VEGF kinase inhibitor, significantly increases cancer cell sensitivity to TRAIL.
  • Down-regulation of the Bcl-2 family protein Mcl-1 by sorafenib is a key mechanism.
  • The combination of TRAIL and sorafenib demonstrates enhanced cancer cell killing.

Conclusions:

  • The TRAIL-sorafenib combination therapy is a promising strategy for overcoming TRAIL resistance.
  • This approach may offer an effective tool against various human cancers.
  • Targeting Mcl-1 in conjunction with TRAIL could improve cancer treatment outcomes.

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