| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2775891 | Experimental and Molecular Pathology | 2007 | 8 Pages |
BackgroundMany colorectal carcinomas are resistant to the growth inhibitory response of transforming growth factor-beta (TGF-β) due to alterations of components along the TGF-β signaling pathway. The aim of this study was to examine the expression of TGF-β1, TβRII and Smad4 in human colorectal carcinoma and their relationships with cancer growth.MethodsImmunohistochemistry and in situ hybridization were performed in 38 cases of colorectal carcinoma.ResultsIntense signal for TGF-β1 protein and TGF-β1 mRNA were found in 71.1% (27/38) and 77.8% (21/27) of colorectal carcinoma, respectively. Intensive TβRII mRNA were detected only in 40% (11/27) cancer tissues (p < 0.05). 65.8% (25/38) of colorectal carcinoma displayed decreased expression in TβRII immunoreactivity staining (p < 0.05). Smad4 protein and Smad4 mRNA were reduced in 63.2% (24/38) and 63% (17/27) of tumors, respectively. Smad4 expression was related to tumor differentiation and Duke's stage (p < 0.05). Furthermore, TGF-β1-positive tumors with lymph node metastasis preferentially had significant reduced Smad4 expression (p < 0.05).ConclusionsDown-regulation of TβRII as well as the over-expression of TGF-β1 play a possible role for the escape of colorectal carcinoma from TGF-β-mediated growth inhibition. Reduced Smad4 is associated with malignancy and progression of colorectal carcinoma.
