NF-κB activation in cancer: A challenge for ubiquitination- and proteasome-based therapeutic approach

Sharon Amit, Yinon Ben-Neriah*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

149 Scopus citations


Nuclear factor-kappa B (NF-κB) activation relies primarily on ubiquitin-mediated degradation of its inhibitor IκB. NF-κB plays an important role in many aspects of tumor development, progression, and therapy. Some types of cancer are characterized by constitutive NF-κB activity, whereas in others such activity is induced following chemotherapy. NF-κB-harboring tumors are generally resistant to chemotherapy and their eradication requires NF-κB inhibition. Here we describe the mechanisms of NF-κB activation in normal and tumor cells, review prevalent notions regarding the factor's contribution to tumorigenicity and discuss present and future options for NF-κB inhibition in cancer. The ubiquitination-mediated activation of NF-κB is intersected by another cancer-associated protein, β-catenin. We, therefore, compare the related activation pathways and discuss the possibility of differential targeting of the involved ubiquitination machinery.

Original languageAmerican English
Pages (from-to)15-28
Number of pages14
JournalSeminars in Cancer Biology
Issue number1
StatePublished - Feb 2003

Bibliographical note

Funding Information:
We are grateful to Drs. Eli Pikarsky and A. Mahler for helpful comments on the manuscript. Supported by the Israel Science Foundation funded by the Israel Academy for Sciences and Humanities-Centers of Excellence Program, the German–Israeli Program (DIP), the European Community (5th framework) and the German–Israeli Foundation for Scientific Research (GIF).


  • Cancer
  • E3
  • IKK
  • NF-κB
  • Proteasome
  • Ubiquitination


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