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The Differential Expressions of the Epithelial-Mesenchymal Transition Regulator, Slug and the Cell Adhesion Molecule, E-cadherin in Colorectal Adenocarcinoma.
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Original Article The Differential Expressions of the Epithelial-Mesenchymal Transition Regulator, Slug and the Cell Adhesion Molecule, E-cadherin in Colorectal Adenocarcinoma.
Ran Hong, Dong Yul Choi, Sung Chul Lim, Chae Hong Suh, Keun Hong Kee, Mi Ja Lee
Journal of Pathology and Translational Medicine 2008;42(6):351-357
DOI: https://doi.org/
1Department of Pathology, College of Medicine, Chosun University, Gwangju, Korea. sclim@chosun.ac.kr
2Research Center for Resistant Cells, College of Medicine, Chosun University, Gwangju, Korea.
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BACKGROUND
Slug is a member of the Snail family of transcription factors, and it plays a crucial role in the regulation of the epithelial-mesenchymal transition by suppression of several epithelial proteins and adhesion molecules, including E-cadherin. METHODS: The aim of the present study was to examine the significance between the expression of Slug in colorectal adenocarcinoma (CRA) specimens and the clinicopathological parameters of CRA, as determined by immunohistochemical analysis, and to determine the correlation between the Slug and E-cadherin expressions in non-neoplastic colorectal mucosa (n=45), primary CRA (n= 109) and metastatic CRA (n=17). A semiquantitative scoring system was applied based on the intensity and extent of the positive immunohistochemical staining. RESULTS: The expressions of Slug and E-cadherin were associated with the depth of tumor invasion (pT) (p=0.019, p=0.001, respectively), and these expressions showed a significant inverse correlation (p<0.001) each other. CONCLUSIONS: Our results demonstrated a positive role for Slug in the development of CRA, and Slug is a mediator of tumor invasion in CRA. In addition, an up-regulated Slug expression is significantly correlated with the loss of an E-cadherin expression, which suggests that Slug may play some role in the epithelial-mesenchymal transition (EMT) by down-regulating the E-cadherin expression.

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