TRAIL resistance results in cancer progression: A TRAIL to perdition?

Research output: Contribution to journalReview articlepeer-review

68 Scopus citations


Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL, APO-2L) is a mediator of cell death that preferentially targets cancer cells. The potential of TRAIL as a chemotherapeutic agent is limited, however, because of the emergence of TRAIL resistance. Furthermore, recent studies have demonstrated that alternative TRAIL signaling is unmasked in TRAIL resistant cells. In these cells, the predominant effect of TRAIL receptor activation is the activation of nuclear factor-κB (NF-κB), which promotes tumor metastases and invasion. TRAIL resistance can occur at the level of the death inducing signaling complex via upregulation of cFLIP or via an increase in antiapoptotic proteins of the Bcl-2 family. A paradigm emerges from this information, that chemotherapy, targeting NF-κB, cFLIP, or antiapoptotic proteins of the Bcl-2 family, in combination with TRAIL maybe more rational than TRAIL therapy alone.

Original languageEnglish (US)
Pages (from-to)7333-7335
Number of pages3
Issue number56
StatePublished - Nov 30 2006


  • Invasion
  • Mcl-1
  • Metastasis
  • NF-κB
  • cFLIP

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Cancer Research


Dive into the research topics of 'TRAIL resistance results in cancer progression: A TRAIL to perdition?'. Together they form a unique fingerprint.

Cite this