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Please use this identifier to cite or link to this item: http://ntour.ntou.edu.tw:8080/ir/handle/987654321/27100

Title: Thymosin beta4 triggers an epithelial–mesenchymal transition in colorectal carcinoma by upregulating integrin-linked kinase
Authors: H-C Huang;C-H Hu;M-C Tang;W-S Wang;P-M Chen;Y Su
Contributors: NTOU:Institute of Bioscience and Biotechnology
Keywords: thymosin beta4;E-cadherin;beta-catenin;integrin-linked kinase;epithelial–mesenchymal transition
Date: 2007
Issue Date: 2011-10-21T02:22:42Z
Publisher: Oncogene
Abstract: Abstract:The epithelial–mesenchymal transition (EMT) is crucial for the invasion and metastasis of many epithelial tumors including colorectal carcinoma (CRC). In the present study, a scattering and fibroblastic morphology with reduced intercellular contacts was found in the SW480 colon cancer cells overexpressing the gene encoding thymosin 4 (T4), which was accompanied by a loss of E-cadherin as well as a cytosolic accumulation of -catenin, two most prominent markers of EMT. Whereas E-cadherin downregulation was likely to be accounted by a ZEB1-mediated transcriptional repression, the accumulation of -catenin was a result of glycogen synthase kinase-3 inactivation mediated by integrin-linked kinase (ILK) and/or its downstream effector, Akt. Intriguingly, ILK upregulation in T4-overexpressing SW480 cells seemed to be attributed mainly to a stabilization of this kinase by complexing with particularly interesting new Cys-His protein (PINCH) more efficiently. In the meantime, a strong correlation between the expression levels of T4, ILK and E-cadherin in CRC patients was also revealed by immunohistochemical analysis. Taken together, these data suggest a novel role of T4 in promoting CRC progression by inducing an EMT in tumor cells via upregulating ILK and consequentially its signal transduction.
Relation: 26, pp.2781–2790
URI: http://ntour.ntou.edu.tw/handle/987654321/27100
Appears in Collections:[生命科學暨生物科技學系] 期刊論文

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