CD133-positive cells are resistant to TRAIL due to up-regulation of FLIP

Biochem Biophys Res Commun. 2008 Sep 5;373(4):567-71. doi: 10.1016/j.bbrc.2008.06.073. Epub 2008 Jun 30.

Abstract

Recent research shows that Cancer stem cells (CSCs) are relatively resistant to apoptosis induction. We studied the effect of the immunological apoptogen TRAIL on Jurkat cells enriched in the CD133-positive population. CD133(high) Jurkat cells were more resistant to apoptosis than their CD133(low) counterparts, and showed higher level of expression of FLIP, an inhibitor of death receptor-mediated apoptosis. Breast cancer MCF7 cells showed high level of expression CD133 in the unseparated culture, with accompanying high level of FLIP. Down-regulation of FLIP by siRNA resulted in sensitisation of the cells to TRAIL, as documented by more robust apoptosis. We conclude that high expression of FLIP is at least one of the reasons for resistance of CSCs to apoptosis induced by the death ligand TRAIL.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • AC133 Antigen
  • Antigens, CD / metabolism*
  • Antineoplastic Agents / pharmacology*
  • Apoptosis*
  • CASP8 and FADD-Like Apoptosis Regulating Protein / metabolism*
  • Glycoproteins / metabolism*
  • Humans
  • Jurkat Cells
  • Neoplastic Stem Cells / drug effects*
  • Neoplastic Stem Cells / metabolism
  • Peptides / metabolism*
  • Recombinant Proteins / pharmacology
  • TNF-Related Apoptosis-Inducing Ligand / pharmacology*
  • Up-Regulation

Substances

  • AC133 Antigen
  • Antigens, CD
  • Antineoplastic Agents
  • CASP8 and FADD-Like Apoptosis Regulating Protein
  • Glycoproteins
  • PROM1 protein, human
  • Peptides
  • Recombinant Proteins
  • TNF-Related Apoptosis-Inducing Ligand
  • TNFSF10 protein, human