期刊
ORGANIC & BIOMOLECULAR CHEMISTRY
卷 15, 期 36, 页码 7623-7629出版社
ROYAL SOC CHEMISTRY
DOI: 10.1039/c7ob01584d
关键词
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资金
- NIH [R01 CA172379]
- Office of the Dean of the College of Medicine
- Center for Pharmaceutical Research and Innovation in the College of Pharmacy
- Department of Defense Idea Development Award from the National Institute of General Medical Sciences [W81XWH-16-1-0635, NIH P20 RR020171]
- National Institutes of Health for the University of Kentucky's Center for Clinical and Translational Science [NIH UL1 TR000117]
- [NIH R21 CA205108]
Cytisine-linked isoflavonoids (CLIFs) inhibited PC-3 prostate and LS174T colon cancer cell proliferation by inhibiting a peroxisomal bifunctional enzyme. A pull-down assay using a biologically active, biotin-modified CLIF identified the target of these agents as the bifunctional peroxisomal enzyme, hydroxysteroid 17 beta-dehydrogenase-4 (HSD17B4). Additional studies with truncated versions of HSD17B4 established that CLIFs specifically bind the C-terminus of HSD17B4 and selectively inhibited the enoyl CoA hydratase but not the D-3-hydroxyacyl CoA dehydrogenase activity. HSD17B4 was overexpressed in prostate and colon cancer tissues, knocking down HSD17B4 inhibited cancer cell proliferation, suggesting that HSD17B4 is a potential biomarker and drug target and that CLIFs are potential probes or therapeutic agents for these cancers.
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