Cytokeratin 18-mediated disorganization of intermediate filaments is induced by degradation of plectin in human liver cells.

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Title:	Cytokeratin 18-mediated disorganization of intermediate filaments is induced by degradation of plectin in human liver cells.
Authors:	趙偉廷 Liu, Yi-Hsiang Ho, Chin-Chin Cheng, Chiung-Chi Chao, Wei-Ting Pei, Ren-Jeng Hsu, Yung-Hsiang Lai, Yih-Shyong
Contributors:	Department of Pathology, Chang Bing Show Chwan Memorial Hospital Department of Pathology, Tzu Chi University Department of Nursing, Central Taiwan University of Science and Technology Department of Medical Research, Chang Bing Show Chwan Memorial Hospital Department of Molecular Physiology and Biophysics, Baylor College of Medicine Yongsin Pathological Center, Taichung
Keywords:	Cytokeratin Cytoskeleton Hepatocellular carcinoma Plectin Staurosporine Transformation
Date:	2011-04
Issue Date:	2016-11-16T02:09:41Z (UTC)
Publisher:	Netherlands:Elsevier
Abstract:	Plectin is a cross-linking protein that organizes the cytoskeleton into a stable meshwork that helps maintain the uniform size and shape of cells. As cells of hepatocellular carcinoma are morphologically different from healthy human hepatocytes, we hypothesized that plectin deficiency and cytoskeletal disorganization underlies this pleomorphic transformation. To test this hypothesis we induced apoptosis as the most accessible pathway for creating plectin deficiency status in vivo. We analyzed expression levels and organization of plectin and other cytoskeletal elements, including intermediate filaments, microfilaments, and microtubules, after staurosporine-induced apoptosis in human Chang liver cells. The results revealed the expression of plectin and cytokeratin 18 were downregulated in hepatocellular carcinoma tissues in vivo. The expression of actin and tubulin, however, were not altered. In vitro analysis indicated that plectin and cytokeratin 18 were cleaved following staurosporine-treatment of human Chang liver cells. Time course experiments revealed that plectin was cleaved 2 h earlier than cytokeratin 18. The organization of plectin and cytokeratin 18 networks collapsed after staurosporine-treatment. Conclusively, degradation of plectin induced by staurosporine-treatment in liver cells resulted in cytoskeleton disruption and induced morphological changes in these cells by affecting the expression and organization of cytokeratin 18.
Relation:	Biochemical and Biophysical Research Communications, 407(3), 575-580
Appears in Collections:	[生命科學系所] 期刊論文

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