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Published on: May 14, 2016

Bcl-X(L) is a chemoresistance factor in human melanoma cells that can be inhibited by antisense therapy

Elisabeth Heere-Ress1, Christiane Thallinger, Trevor Lucas

  • 1Department of Clinical Pharmacology, Section of Experimental Oncology/Molecular Pharmacology, University of Vienna, Vienna, Austria.

International Journal of Cancer
|April 12, 2002
PubMed

Insights

Bcl-x(L) protein promotes chemoresistance in malignant melanoma. Reducing Bcl-x(L) levels with antisense oligonucleotides enhances chemotherapy effectiveness, offering a promising strategy to overcome treatment resistance in melanoma patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Therapeutics

Background:

  • Malignant melanoma exhibits poor response to apoptosis-inducing chemotherapy.
  • Gene expression regulating apoptotic cell death influences tumor cell sensitivity to chemotherapy.
  • Bcl-x(L), an antiapoptotic protein, is consistently expressed in human melanoma.

Purpose of the Study:

  • To investigate Bcl-x(L) as a potential therapeutic target in melanoma.
  • To determine the impact of Bcl-x(L) expression levels on human melanoma cell chemoresistance.

Main Methods:

  • Stable transfection of human melanoma Mel Juso cells to overexpress Bcl-x(L).
  • Treatment with antisense (AS) oligonucleotide (ISIS 16009) to reduce Bcl-x(L) protein levels.
  • Assessment of cisplatin-induced apoptosis and chemosensitivity.

Main Results:

  • Overexpression of Bcl-x(L) significantly decreased sensitivity to cisplatin-induced apoptosis (p < 0.05).
  • AS oligonucleotide treatment enhanced Mel Juso cell chemosensitivity by 62% compared to control oligonucleotide.
  • Reduced Bcl-x(L) expression potentiated chemotherapy-induced apoptosis.

Conclusions:

  • Bcl-x(L) is a key contributor to chemoresistance in human melanoma.
  • Targeting Bcl-x(L) expression with AS oligonucleotides is a rational and promising approach.
  • This strategy may help overcome chemoresistance in melanoma treatment.

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