Targeting neddylation effectively antagonizes nuclear factor-κB in chronic lymphocytic leukemia B-cells

Leuk Lymphoma. 2015 May;56(5):1566-9. doi: 10.3109/10428194.2014.990901.

Abstract

Chronic lymphocytic leukemia (CLL) B-cells demonstrate both constitutive and stroma-mediated activation of nuclear factor-κB (NF-κB). NEDD8, a ubiquitin-like protein, regulates activity of Cullin-RING ubiquitin ligases (CRLs) and thus indirectly controls NF-κB activity. Inhibition of CRLs with MLN4924, an investigational agent that targets the NEDD8-activating enzyme, induces accumulation of CRL substrates, including inhibitor of NF-κB (IκB), a negative pathway modulator. We demonstrate that both continuous and pulse treatments with MLN4924 abrogate NF-κB activity in CLL B-cells ex vivo in a CD40L-expressing stromal co-culture system and identify pathways potentially responsible for resistance to MLN4924. To achieve long-lasting therapeutic effects in CLL, combination strategies are likely necessary.

Keywords: Chronic lymphocytic leukemia; MLN4924; NF-κB; neddylation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / drug effects
  • Cell Line, Tumor
  • Cyclopentanes / pharmacology
  • Gene Expression Regulation, Leukemic / drug effects
  • Humans
  • Leukemia, Lymphocytic, Chronic, B-Cell / genetics
  • Leukemia, Lymphocytic, Chronic, B-Cell / metabolism*
  • NEDD8 Protein
  • NF-kappa B / antagonists & inhibitors
  • NF-kappa B / metabolism*
  • Pyrimidines / pharmacology
  • Transcription, Genetic
  • Ubiquitins / metabolism

Substances

  • Cyclopentanes
  • NEDD8 Protein
  • NEDD8 protein, human
  • NF-kappa B
  • Pyrimidines
  • Ubiquitins
  • pevonedistat