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Selenium supplementation modulates collagen type I alpha 1 gene expression in cultured prostate cells
Author(s) -
FairweatherTait Susan Jane,
Hurst Rachel
Publication year - 2007
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.21.5.a718-a
Subject(s) - selenium , lncap , gene expression , chemistry , gene , prostate cancer , alpha (finance) , biology , cancer research , microbiology and biotechnology , cancer , biochemistry , genetics , medicine , construct validity , nursing , organic chemistry , patient satisfaction
Selenium and its anti‐cancer effects have been demonstrated to be form specific and dose dependent. Se‐methylselenocysteine (MSC) is one of the most effective anti‐carcinogenic forms of selenium. Our aim was to study the mechanistic effects of supplementation with MSC in prostate cells in relation to protection against cancer. We exposed cell lines (LNCap and PNT1A) to physiologically relevant doses of selenium ranging from deficiency through to adequate, and the equivalent of a selenium supplement dose in humans. The cells were adapted to the various selenium doses for one month in order to attain steady‐state selenium status. Two microarray platforms were used to probe the molecular effects of selenium dose and form on prostate cells and several selenium‐responsive genes were identified that may be involved in cancer prevention. One gene that significantly changed in response to selenium dose and form was collagen type I alpha 1 (COL1A1). We designed and validated a real time RT‐PCR assay to confirm changes in COL1A1 gene expression, and observed significantly reduced levels of mRNA expression in the selenium supplemented cells compared to the control cells. The novel gene expression changes identified will be investigated further; we are currently studying the effect of selenium on collagen type I protein expression to investigate the functional significance of the changes in gene expression. Supported by the BBSRC, UK.

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