论文部分内容阅读
Objective: Smad7 was identified as a TGF-b-inducible antagonist of TGF-b signaling and might participate in a negative feedback loop to control TGF-b signaling. In this study, the responsiveness of Smad7 to TGF-b1 wasexamined in the BEP2D and BERP35T-2 cells to investigate the possible mechanism of Smad7 in the tumorigenesis.Methods: Northern and western blot were performed toexam the Smad7 and TGF-b1 expression abundance inBEP2D and BERP35T-2 at both transcription andtranslation level. Results: The expression level of Smad7 mRNA in BERP35T-2 cells was higher than that in BEP2D cells. When stimulated with TGF-b1, Smad7 expression was up-regulated evidently in BEP2D cells, but not significantly in BERP35T-2 cells. The abundance of TGF-b1 in thecytoplasm of BERP35T-2 was not significantly higher than in BEP2D (P>0.05); whereas the abundance of TGF-b1 in BERP35T-2 cell culture medium was significantly higherthan in BEP2D cell culture medium (P<0.05). Conclusion: Over expression of Smad7 mRNA and down-regulation of the cells’ responsiveness to TGF-b1 in human lung cancer cell line might be involved in lung carcinogenisis.
Objective: Smad7 was identified as a TGF-b-inducible antagonist of TGF-b signaling and might participate in a negative feedback loop to control TGF-b signaling. In this study, the responsiveness of Smad7 to TGF-b1 wasexamined in the BEP2D and BERP35T-2 cells to investigate the possible mechanism of Smad7 in the tumorigenesis. Methods: Northern and western blot were performed to express the Smad7 and TGF-b1 expression abundance in BEEP2D and BERP35T-2 at both transcription and translation level. Results: The expression level of Smad7 When stimulated with TGF-b1, Smad7 expression was up-regulated evidently in BEP2D cells, but not significantly in BERP35T-2 cells. The abundance of TGF-b1 in the cytoplasm of BERP35T-2 was not significantly higher than in BEP2D (P> 0.05); while the abundance of TGF-b1 in BERP35T-2 cell culture medium was significantly higherthan in BEP2D cell culture medium d7 mRNA and down-regulation of the cells’ responsiveness to TGF-b1 in human lung cancer cell line might be involved in lung carcinogenisis.