期刊
FASEB JOURNAL
卷 30, 期 8, 页码 2812-+出版社
FEDERATION AMER SOC EXP BIOL
DOI: 10.1096/fj.201600251R
关键词
selenoprotein; NF kappa B; colorectal; cytokeratin; nutrigenomics
资金
- Newcastle Healthcare Charity
- Biotechnology and Biological Sciences Research Council (BBSRC) [BB/H011471/1]
- United Kingdom Food Standards Agency [N12015]
- BBSRC
- Biotechnology and Biological Sciences Research Council [BB/H011471/1]
- BBSRC [BB/H011471/1, BBS/E/F/00042195] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/H011471/1, BBS/E/F/00042195] Funding Source: researchfish
Epidemiologic studies highlight the potential role of dietary selenium (Se) in colorectal cancer prevention. Our goal was to elucidate whether expression of factors crucial for colorectal homoeostasis is affected by physiologic differences in Se status. Using transcriptomics and proteomics followed by pathway analysis, we identified pathways affected by Se status in rectal biopsies from 22 healthy adults, including 11 controls with optimal status (mean plasma Se = 1.43 mu M) and 11 subjects with suboptimal status (mean plasma Se = 0.86 mu M). We observed that 254 genes and 26 proteins implicated in cancer (80%), immune function and inflammatory response (40%), cell growth and proliferation (70%), cellular movement, and cell death (50%) were differentially expressed between the 2 groups. Expression of 69 genes, including selenoproteins W1 and K, which are genes involved in cytoskeleton remodelling and transcription factor NF kappa B signaling, correlated significantly with Se status. Integrating proteomics and transcriptomics datasets revealed reduced inflammatory and immune responses and cytoskeleton remodelling in the suboptimal Se status group. This is the first study combining omics technologies to describe the impact of differences in Se status on colorectal expression patterns, revealing that suboptimal Se status could alter inflammatory signaling and cytoskeleton in human rectal mucosa and so influence cancer risk.
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