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Is there a role for nuclear factor kappaB in tumor necrosis factor-related apoptosis-inducing ligand resistance?

Amandine Plantivaux1, Eva Szegezdi, Afshin Samali

  • 1Department of Pharmacology and Therapeutics, National University of Ireland, Galway, Ireland.

Annals of the New York Academy of Sciences
|September 3, 2009
PubMed

Insights

This review examines how nuclear factor-kappaB (NF-κB) may contribute to cancer cells resisting Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand (TRAIL) therapy. Understanding this resistance mechanism is crucial for improving cancer treatment strategies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Selective apoptosis induction in cancer cells is a key strategy for cancer management.
  • Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand (TRAIL) is a promising anticancer agent due to its selective cancer cell apoptosis-inducing properties.
  • Many tumors exhibit resistance to TRAIL-mediated apoptosis, necessitating investigation into underlying mechanisms.

Purpose of the Study:

  • To review and summarize current data on the involvement of the transcription factor nuclear factor-kappaB (NF-κB) in TRAIL resistance.
  • To elucidate the potential role of NF-κB in mediating resistance to TRAIL-based cancer therapies.

Main Methods:

  • Literature review of studies investigating TRAIL resistance in cancer.
  • Analysis of data linking nuclear factor-kappaB (NF-κB) activity to TRAIL sensitivity or resistance.
  • Synthesis of findings regarding the molecular mechanisms of NF-κB in TRAIL resistance.

Main Results:

  • Evidence suggests a significant role for nuclear factor-kappaB (NF-κB) in conferring resistance to TRAIL-induced apoptosis in various cancer types.
  • NF-κB activation can upregulate anti-apoptotic proteins and interfere with TRAIL signaling pathways.
  • The precise mechanisms and extent of NF-κB involvement in TRAIL resistance are complex and context-dependent.

Conclusions:

  • Nuclear factor-kappaB (NF-κB) is implicated as a key mediator of TRAIL resistance in cancer.
  • Targeting NF-κB signaling pathways may represent a viable strategy to overcome TRAIL resistance and enhance the efficacy of TRAIL-based cancer therapies.
  • Further research is warranted to fully understand and therapeutically exploit the NF-κB-TRAIL resistance axis.

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