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Thymosin β4 triggers an epithelial–mesenchymal transition in colorectal carcinoma by upregulating integrin-linked kinase

Thymosin β4 triggers an epithelial–mesenchymal transition in colorectal carcinoma by upregulating... 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 β4 (Tβ 4), which was accompanied by a loss of E-cadherin as well as a cytosolic accumulation of β-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 β-catenin was a result of glycogen synthase kinase-3β inactivation mediated by integrin-linked kinase (ILK) and/or its downstream effector, Akt. Intriguingly, ILK upregulation in Tβ 4-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 Tβ 4, ILK and E-cadherin in CRC patients was also revealed by immunohistochemical analysis. Taken together, these data suggest a novel role of Tβ 4 in promoting CRC progression by inducing an EMT in tumor cells via upregulating ILK and consequentially its signal transduction. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Oncogene Springer Journals

Thymosin β4 triggers an epithelial–mesenchymal transition in colorectal carcinoma by upregulating integrin-linked kinase

Huang, H-C; Hu, C-H; Tang, M-C; Wang, W-S; Chen, P-M; Su, Y
Oncogene , Volume 26 (19) – Oct 30, 2006
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References (64)

Publisher
Springer Journals
Copyright
Copyright © 2007 by Nature Publishing Group
Subject
Medicine & Public Health; Medicine/Public Health, general; Internal Medicine; Cell Biology; Human Genetics; Oncology; Apoptosis
ISSN
0950-9232
eISSN
1476-5594
DOI
10.1038/sj.onc.1210078
Publisher site
See Article on Publisher Site

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 β4 (Tβ 4), which was accompanied by a loss of E-cadherin as well as a cytosolic accumulation of β-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 β-catenin was a result of glycogen synthase kinase-3β inactivation mediated by integrin-linked kinase (ILK) and/or its downstream effector, Akt. Intriguingly, ILK upregulation in Tβ 4-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 Tβ 4, ILK and E-cadherin in CRC patients was also revealed by immunohistochemical analysis. Taken together, these data suggest a novel role of Tβ 4 in promoting CRC progression by inducing an EMT in tumor cells via upregulating ILK and consequentially its signal transduction.

Journal

Oncogene – Springer Journals

Published: Oct 30, 2006

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