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C-Myc is a Nrf2-interacting protein that negatively regulates phase II genes through their electrophile responsive

Smadar Levy1, Henry Jay Forman

  • 1Department of Natural Sciences, University of California, Merced, USA.

IUBMB Life
|March 17, 2010
PubMed

Insights

The transcription factor c-Myc negatively regulates phase II genes by interacting with the electrophile response element (EpRE) and decreasing Nrf2 stability, impacting cancer and cellular processes.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Biochemistry

Background:

  • c-Myc is a key transcription factor regulating cell proliferation, apoptosis, and cancer.
  • Previous studies linked c-Myc to glutamate cysteine ligase regulation via E-box sequences.
  • The role of c-Myc in regulating phase II genes through the electrophile response element (EpRE) was unexplored.

Purpose of the Study:

  • To investigate whether c-Myc regulates phase II genes via interaction with the electrophile response element (EpRE).

Main Methods:

  • Experiments utilized human bronchial epithelial cells with si-RNA to knock down c-Myc.
  • Quantitative reverse transcription PCR (RT-PCR) and reporter assays measured gene transcription and promoter activity.
  • Chromatin immunoprecipitation (ChIP) and co-immunoprecipitation (Co-IP) assays assessed protein interactions and DNA binding.

Main Results:

  • c-Myc was found to downregulate the transcription and promoter activity of phase II genes.
  • Chromatin immunoprecipitation confirmed c-Myc binding to the EpRE.
  • Co-immunoprecipitation showed c-Myc interacts with Nrf2, forming a ternary complex with p-c-Jun, and decreases Nrf2 stability.

Conclusions:

  • c-Myc negatively regulates the EpRE/Nrf2 signaling pathway.
  • This regulation occurs through direct interaction with the EpRE binding complex and by increasing Nrf2 degradation.
  • These findings elucidate a novel mechanism of c-Myc-mediated gene regulation relevant to cancer and cellular defense.

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