Journal
BIOCHEMICAL JOURNAL
Volume 423, Issue -, Pages 315-321Publisher
PORTLAND PRESS LTD
DOI: 10.1042/BJ20091170
Keywords
cancer; cytokine; inflammation; isothiocyanate (ITC); macrophage migration inhibitory factor (MIF); tautomerase
Categories
Funding
- National Institutes of Health [R01AT004323, R01 CA113899]
- American Cancer Center [IRG81-001-23]
Ask authors/readers for more resources
Dietary ITCs (isothiocyanates) prevent cancer and show other bioactivities in vivo. As electrophiles, ITCs may covalently modify cellular proteins. Using a novel proteomics screen, we identified MIF (macrophage migration inhibitory factor) as the principal target of nutrient ITCs in intact cells. ITCs covalently modify the N-terminal proline residue of MIF and extinguish its catalytic tautomerase activity. MIF deficiency does not prevent induction of Phase 2 gene expression, a hallmark of many cancer chemopreventives, including ITCs. Due to the emerging role of MIF in the control of malignant cell growth and its clear involvement in inflammation, inhibition of MIF by nutrient ITCs suggests therapeutic strategies for inflammatory diseases and cancer.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available