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Regulation of cytochrome P450 4F11 by nuclear transcription factor-κB

Jordan C Bell1, Henry W Strobel

  • 1Department of Biochemistry and Molecular Biology, University of Texas-Houston Medical School, 6431 Fannin St., Houston, TX 77225, USA.

Drug Metabolism and Disposition: the Biological Fate of Chemicals
|October 21, 2011
PubMed

Insights

Nuclear factor-kappa B (NF-κB) inhibits CYP4F11 gene expression. This study demonstrates NF-κB

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Genetics

Background:

  • CYP4F gene regulation mechanisms are not fully understood.
  • Tumor necrosis factor-alpha (TNF-α) activates NF-κB and JNK signaling.
  • JNK signaling is reported to up-regulate CYP4F11 expression.

Purpose of the Study:

  • To investigate the role of NF-κB in regulating CYP4F11 expression.
  • To elucidate the interaction between TNF-α, NF-κB, and JNK signaling in CYP4F11 regulation.

Main Methods:

  • Utilized HepG2 human liver carcinoma cell line.
  • Employed NF-κB translocation inhibitor IMD-0354.
  • Performed gene knockdown of p65 (NF-κB protein) and promoter activity assays.

Main Results:

  • TNF-α with an NF-κB inhibitor showed increased CYP4F11 expression compared to TNF-α alone.
  • NF-κB stimulation via kinase overexpression inhibited CYP4F11 promoter activity.
  • p65 knockdown rescued CYP4F11 promoter inhibition in the presence of TNF-α.

Conclusions:

  • NF-κB signaling pathways negatively regulate the CYP4F11 gene.
  • NF-κB acts as an inhibitor of CYP4F11 expression, contrasting with JNK pathway effects.

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