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Mcl-1 blocks radiation-induced apoptosis and inhibits clonogenic cell death

Hans Skvara1, Christiane Thallinger, Volker Wacheck

  • 1Department of Radiotherapy and Radiobiology, University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria.

Anticancer Research
|August 6, 2005
PubMed
Abstract

Insights

Mcl-1 (myeloid cell leukemia 1) protein expression increases radioresistance in human melanoma cells. Down-regulating Mcl-1 with antisense oligonucleotides enhances cell death when combined with ionizing radiation.

Area of Science:

  • Oncology
  • Molecular Biology
  • Radiotherapy

Background:

  • Anti-apoptotic Bcl-2 family proteins, like Bcl-2 and Bcl-x, influence cancer treatment sensitivity.
  • The role of Mcl-1 (myeloid cell leukemia 1) in tumor cell response to ionizing radiation (IR) was previously unknown.

Purpose of the Study:

  • To investigate the relationship between Mcl-1 expression and the radioresponse of human melanoma cells.
  • To determine if Mcl-1 plays a role in radioresistance.

Main Methods:

  • Human melanoma cells were treated with Mcl-1 antisense oligonucleotides (ASOs) and IR.
  • Evaluated effects on proliferation, apoptosis, and clonogenic cell death.

Main Results:

  • Combined ASO treatment and IR reduced cell numbers 9.5-fold, significantly more than ASO or IR alone.
  • Apoptosis increased to 49% in combined treatment groups versus controls.
  • Colony formation assays showed a synergistic effect between Mcl-1 down-regulation and IR.

Conclusions:

  • Mcl-1 expression significantly impacts the radioresistance of human melanoma cells.
  • Targeting Mcl-1 may enhance the efficacy of radiotherapy for melanoma.

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