Analytical Cellular Pathology

Analytical Cellular Pathology / 2009 / Article

Open Access

Volume 31 |Article ID 975602 | https://doi.org/10.3233/CLO-2009-0460

Vasiliki Bravou, Anna Antonacopoulou, Helen Papadaki, Konstantina Floratou, Michalis Stavropoulos, Vasso Episkopou, Chariklia Petropoulou, Haralabos Kalofonos, "TGF-β Repressors SnoN and Ski Are Implicated in Human Colorectal Carcinogenesis", Analytical Cellular Pathology, vol. 31, Article ID 975602, 11 pages, 2009. https://doi.org/10.3233/CLO-2009-0460

TGF-β Repressors SnoN and Ski Are Implicated in Human Colorectal Carcinogenesis

Abstract

Background: The TGF-β signaling repressors SnoN and Ski have been critically implicated in human cancer.Methods: To explore the role of SnoN and Ski in the development and progression of colorectal cancer we examined their protein expression profile by immunohistochemistry in a series of human colorectal adenomas, carcinomas and lymph node metastases. The mRNA expression of SnoN was also quantified by Real-Time RT-PCR.Results: SnoN and Ski were overexpressed both in adenomas with severe dysplasia and colorectal carcinomas. Protein expression was cytoplasmic and nuclear with predominant cytoplasmic localization. The subcellular localization was related differently to pathologic variables of colorectal carcinomas. Although there was no significant association of protein levels with tumor invasion and metastasis, a significant correlation of nuclear SnoN and Ski with β-catenin pathway was observed. Moreover, SnoN mRNA did not differ in carcinomas as compared to normal control and there was no correlation between SnoN protein and mRNA levels.Conclusion: Our findings suggest that SnoN and Ski exert oncogenic effects in human colorectal carcinogenesis and their overexpression is implicated in early stage disease.

Copyright © 2009 Hindawi Publishing Corporation and the authors. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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