Transient knockdown-mediated deficiency in plectin alters hepatocellular motility in association with activated FAK and Rac1-GTPase.

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Title:	Transient knockdown-mediated deficiency in plectin alters hepatocellular motility in association with activated FAK and Rac1-GTPase.
Authors:	趙偉廷 Cheng, Chiung-Chi Lai, Yen-Chang Clark Lai, Yih-Shyong Hsu, Yung-Hsiang Chao, Wei-Ting Sia, Kee-Chin Tseng, Yu-Hui Liu, Yi-Hsiang
Contributors:	Department of Pathology, Chang Bing Show Chwan Memorial Hospital Center for General Education, Providence University Department of Pathology, Kaohsiung Medical University Hospital Department of Pathology, Tzu Chi University Department of Life Science, Tunghai University
Keywords:	Cell motility Cytoskeleton Focal adhesion kinase Hepatocellular carcinoma Plectin
Date:	2015-03
Issue Date:	2016-11-10T01:39:06Z (UTC)
Publisher:	BioMed Central
Abstract:	Background Plectin is one of the cytolinker proteins that play a crucial role in maintaining the integrity of cellular architecture. It is a component of desmosome complexes connecting cytoskeletal proteins and trans-membrane molecules. In epithelial cells, plectin connects cytokeratins and integrin α6β4 in hemidesmosomes anchoring to the extracellular matrix. In addition to the function of molecular adherent, plectin has been reported to exhibit functions affecting cellular signals and responsive activities mediated by stress, cellular migration, polarization as well as the dynamic movement of actin filaments. Plectin deficiency in hepatocellular carcinoma results in abnormal expression of cytokeratin 18 and disassembled hemidesmosome. Therefore, it is hypothesized that the plectin deficiency-mediated collapse of cytoskeleton may modulate cellular motility that is associated with consequent metastatic behaviors of cancer cells. Methods and results The cellular motility of plectin-deficient Chang liver cells generated by transient knockdown were analyzed by trans-well migration assay and the results revealed a higher migration rate. The confocal microscopy also demonstrated less organized and more polarized morphology as well as more focal adhesion kinase activity in comparison with that of the mock Chang liver cells. Furthermore, plectin-knockdown in Chang liver cells was associated with a higher activity of Rac1-GTPase in accordance with the results of the Rac1 pull-down assay. The immunohistochemical assay on human hepatocellular carcinoma showed that the expression of focal adhesion kinase was increased in the invasive front of tumor. Conclusion Plectin-deficient human hepatic cells exhibit higher cell motility associated with increase in focal adhesion kinase activity that are comparable to the properties of invasive hepatocellular carcinoma.
Relation:	Cancer cell international, 15(29), 1-7
Appears in Collections:	[生命科學系所] 期刊論文

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