Premium
Effect of Dietary Bioactive Compounds on Thioredoxin Reductase 1 and 15kDa Selenoprotein Expression in Colon Cancer Cells
Author(s) -
Rosso Lauren,
Galinn Sarah,
Carlson Bradley,
Tobe Ryuta,
NaranjoSuarez Salvador,
Tsuji Petra
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.759.8
Subject(s) - sulforaphane , resveratrol , selenoprotein , thioredoxin reductase , thioredoxin , carcinogenesis , chemistry , pregnane x receptor , microbiology and biotechnology , biochemistry , cancer research , oxidative stress , biology , nuclear receptor , transcription factor , catalase , gene , glutathione peroxidase
Many selenoproteins are involved in cellular homeostasis, protecting normal and cancer cells from oxidative stress. Thus, some selenoproteins are thought to have roles in both preventing and promoting cancer. We compared the effects of sulforaphane, resveratrol and several flavones on the expression of thioredoxin reductase 1 (TR1) and the 15kDa selenoprotein (Sep15) in HT29 human colon cancer cells to further elucidate the regulatory mechanisms involved with these two selenoproteins. Nrf2‐regulated TR1 mRNA was increased by sulforaphane as expected, but increased by 5‐hydroxy‐7‐methoxyflavone and resveratrol only in shSep15 cells. In contrast, Sep15 mRNA was decreased by up to 50% when cells were exposed to 5‐methoxyflavone, 5‐hydroxy‐7‐methoxyflavone, 7‐hydroxyflavone or resveratrol, which are known to affect aryl hydrocarbon receptor signaling. Surprisingly, sulforaphane decreased Sep15 mRNA expression in shTR1 cells. Our preliminary results suggest that dietary compounds may affect various molecular pathways, resulting in differential and possibly antagonistic regulation of Sep15 and TR1. Intriguingly, some compensatory expression may be possible between these two selenoproteins. Additionally, our results may help identify whether these dietary compounds may have an impact on carcinogenesis, and thus may be used as preventive measures against colon tumorigenesis. Funding: National Cancer Institute Intramural support, Towson University Jess & Mildred Fisher Endowed Chair (PAT), and a Towson University Undergraduate Research Grant (LER)