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Type: Journal article
Title: Intracellular zinc depletion induces caspase activation and p21Waf1/Cip1 cleavage in human epithelial cell lines
Author: Chai, F.
TruongTran, A.
Evdokiou, A.
Young, G.
Zalewski, P.
Citation: Journal of Infectious Diseases, 2000; 182(Suppl 1):S85-S92
Publisher: University of Chicago Press
Issue Date: 2000
ISSN: 0022-1899
Statement of
F. Chai, A. Q. Truong-Tran, A. Evdokiou, G. P. Young and P. D. Zalewski
Abstract: To better understand the mechanisms by which zinc deficiency induces epithelial cell death, studies were done of the effects of intracellular zinc depletion induced by the zinc chelator TPEN on apoptosis-related events in human malignant epithelial cell lines LIM1215 (colonic), NCI-H292 (bronchial), and A549 (alveolar type II). In TPEN-treated cells, depletion of zinc was followed by activation of caspase-3 (as demonstrated by enzymatic assay and Western blotting), DNA fragmentation, and morphologic changes. Increase in caspase-3 activity began 1–2 h after addition of TPEN, suggesting that zinc may suppress a step just before the activation of this caspase. Caspase-6, a mediator of caspase-3 processing, also increased, but later than caspase-3. Effects of TPEN on apoptosis were completely prevented by exogenous ZnSO4 and partially prevented by peptide caspase inhibitors. A critical substrate of caspase-3 may be the cell cycle regulator p21Waf1/Cip1, which was rapidly cleaved in TPEN-treated cells to a 15-kDa fragment before further degradation.
Keywords: Tumor Cells, Cultured
Epithelial Cells
Chelating Agents
Enzyme Inhibitors
Cysteine Proteinase Inhibitors
DNA Fragmentation
Cyclin-Dependent Kinase Inhibitor p21
Caspase 3
Caspase 6
Rights: © 2000 by the Infectious Diseases Society of America. All rights reserved.
DOI: 10.1086/315914
Appears in Collections:Aurora harvest 5
Orthopaedics and Trauma publications

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