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Targeted deletion of Cyp24a1 in the intestine reduces mucosal injury and preserves epithelial proliferation after 5-fluorouracil treatment.
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Vitamin D has been proposed to attenuate chemotherapy-induced gastrointestinal mucositis (GM). In the intestine, local catabolism of active vitamin D [1,25-dihydroxyvitamin D₃] is mediated by the enzyme Cyp24a1. This study assessed whether deletion of Cyp24a1 specifically in intestinal epithelial cells can protect against 5-fluorouracil (5-FU)-induced intestinal injury and microbiome disruption in mice.
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United European Gastroenterol J
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Sheba Medical Center Tel Hashomer, Faculty of Medical and Health Sciences, Gastroenterology Institute, Tel-Aviv University, Tel Aviv, Israel.
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View Article and Find Full Text PDFPirin does not bind to p65 or regulate NFκB-dependent gene expression but does modulate cellular quercetin levels.
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Department of Pharmacology and Toxicology, Michigan State University, East Lansing, Michigan; "Nicholas V. Perricone, M.D.," Division of Dermatology, Department of Medicine, Michigan State University, East Lansing, Michigan. Electronic address:
Pirin is a nonheme iron-binding protein with a variety of proposed functions, including serving as a coactivator of p65 NFκB and quercetinase activity. We report here, failure to confirm pirin's primary proposed mechanism, binding of Fe(III)-pirin and p65. Analytical size exclusion chromatography and fluorescence polarization studies did not detect an interaction.
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View Article and Find Full Text PDFAntrocinol-Mediated Downregulation of ATG5 Induces Autophagy-Dependent Cell Death and Activates the Unfolded Protein Response Through PERK/CHOP Signaling in Lenvatinib-Resistant Hepatocellular Carcinoma Cells.
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Department of Emergency Medicine, Shuang-Ho Hospital, Taipei Medical University, New Taipei City, Taiwan; Department of Emergency Medicine, School of Medicine, Taipei Medical University, Taipei, Taiwan. Electronic address:
Background: This study seeks to provide preclinical evidence demonstrating the potential of Antrocinol, a derivative of antrocin derived from the active compound of Antrodia cinnamomea, as a promising small-molecule drug candidate for overcoming drug-resistant hepatocellular carcinoma (HCC).
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