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Selenomethionine regulates cyclooxygenase-2 (COX-2) expression through nuclear factor-kappa B (NF-kappaB) in colon

Durga P Cherukuri1, Anne-Christine Goulet, Hiroyasu Inoue

  • 1Department of Pathology, Arizona Cancer Center, The University of Arizona College of Medicine, Tucson, Arizona 85724, USA.

Cancer Biology & Therapy
|January 19, 2005
PubMed

Insights

Selenomethionine (Se-Met) inhibits colon cancer cell growth by suppressing COX-2. This study reveals Se-Met modulates the nuclear factor-kappa B (NF-kappaB) pathway, reducing NF-kappaB

Area of Science:

  • Oncology
  • Molecular Biology
  • Nutritional Science

Background:

  • Selenomethionine (Se-Met) previously demonstrated inhibition of colon cancer cell growth by reducing COX-2 expression.
  • The precise molecular mechanisms underlying Se-Met's suppression of COX-2 require further investigation.

Purpose of the Study:

  • To elucidate the molecular mechanism by which Se-Met suppresses COX-2 expression in colon cancer cells.
  • To investigate the role of nuclear factor-kappa B (NF-kappaB) in Se-Met's regulation of COX-2.

Main Methods:

  • Colon cancer HCA-7 cells were transfected with COX-2 promoter constructs.
  • Cells were treated with Se-Met (90 microM) and analyzed for NF-kappaB activity.
  • Electrophoretic mobility shift assays (EMSA) and supershift assays were performed.

Main Results:

  • Se-Met treatment led to the inhibition of COX-2 at the transcriptional level.
  • NF-kappaB was identified as a key transcription factor involved in COX-2 regulation.
  • Se-Met significantly inhibited NF-kappaB DNA binding activity and nuclear translocation of the p65 subunit.

Conclusions:

  • Se-Met suppresses COX-2 expression in colon cancer cells by modulating NF-kappaB transcriptional activity.
  • The findings suggest a novel mechanism involving NF-kappaB inhibition by Se-Met for colon cancer therapy.

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