OBJECTIVE: To study the functional role of transforming growth factor beta1(TGFbeta1) in the regulation of epithelial-mesenchymal transition (EMT) and the effect of TGFbeta1-ASODN blockage of EMT in esophagus squamous cell carcinoma. METHODS: Esophageal squamous cell carcinoma cell line EC9706 was transfected with chemically synthesized TGFbeta1-ASODN. RT-PCR, immunohistochemistry and flow cytometry were used to detect the protein and mRNA expressions of TGF-beta1, E-cadherin and vimentin before and after the transfection. Morphological changes were documented and scarification test was used to detect the migration potential of EC9706 before and after the transfection. RESULTS: After TGFbeta1-ASODN transfection, mRNA (0.25 +/- 0.07) and protein (35.07% +/- 1.42%) expressions of TGFbeta1 in EC9706 were significantly lower than those before transfection (mRNA: 0.43 +/- 0.09; protein: 43.57% +/- 1.77%, chi(2) = 13.847 and chi(2) = 84.120, P < 0.05). The mRNA (0.38 +/- 0.09) and protein (17.13% +/- 1.45%) expressions of E-cadherin were significantly higher than those before transfection (0.22 +/- 0.06; 12.53% +/- 1.31%, chi(2) = 0.160 and chi(2) = 40.008, P < 0.05) and the mRNA (0.73 +/- 0.07) and protein (14.15% +/- 1.46%) expressions of vimentin were significantly lower than those (0.89 +/- 0.09; 17.97% +/- 1.42%) before transfection (chi(2) = 0.160 and chi(2) = 21.103, P < 0.05). Scarification test showed that after transfection, the mobility of EC9706 was significantly inhibited and its migration length (0.45 +/- 0.05) was significantly shorter than that before the transfection (0.81 +/- 0.11, chi(2) = 16.854, P < 0.05). CONCLUSIONS: TGFbeta1 may contribute to EMT in esophageal squamous cell carcinoma. TGFbeta1-ASODN leads to an over-expression of E-cadherin and a down-regulation of vimentin, along with the morphological alterations and migration inhibition, indicating that a blockage of TGFbeta1 suppresses EMT in esophagus squamous cell carcinoma.
OBJECTIVE: To study the functional role of transforming growth factor beta1(TGFbeta1) in the regulation of epithelial-mesenchymal transition (EMT) and the effect of TGFbeta1-ASODN blockage of EMT in esophagus squamous cell carcinoma. METHODS:Esophageal squamous cell carcinoma cell line EC9706 was transfected with chemically synthesized TGFbeta1-ASODN. RT-PCR, immunohistochemistry and flow cytometry were used to detect the protein and mRNA expressions of TGF-beta1, E-cadherin and vimentin before and after the transfection. Morphological changes were documented and scarification test was used to detect the migration potential of EC9706 before and after the transfection. RESULTS: After TGFbeta1-ASODN transfection, mRNA (0.25 +/- 0.07) and protein (35.07% +/- 1.42%) expressions of TGFbeta1 in EC9706 were significantly lower than those before transfection (mRNA: 0.43 +/- 0.09; protein: 43.57% +/- 1.77%, chi(2) = 13.847 and chi(2) = 84.120, P < 0.05). The mRNA (0.38 +/- 0.09) and protein (17.13% +/- 1.45%) expressions of E-cadherin were significantly higher than those before transfection (0.22 +/- 0.06; 12.53% +/- 1.31%, chi(2) = 0.160 and chi(2) = 40.008, P < 0.05) and the mRNA (0.73 +/- 0.07) and protein (14.15% +/- 1.46%) expressions of vimentin were significantly lower than those (0.89 +/- 0.09; 17.97% +/- 1.42%) before transfection (chi(2) = 0.160 and chi(2) = 21.103, P < 0.05). Scarification test showed that after transfection, the mobility of EC9706 was significantly inhibited and its migration length (0.45 +/- 0.05) was significantly shorter than that before the transfection (0.81 +/- 0.11, chi(2) = 16.854, P < 0.05). CONCLUSIONS:TGFbeta1 may contribute to EMT in esophageal squamous cell carcinoma. TGFbeta1-ASODN leads to an over-expression of E-cadherin and a down-regulation of vimentin, along with the morphological alterations and migration inhibition, indicating that a blockage of TGFbeta1 suppresses EMT in esophagus squamous cell carcinoma.