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Responsiveness of Smad7 gene to TGF-β1 in the tumorigenesis

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Chinese Journal of Cancer Research

Abstract

Objective: Smad7 was identified as a TGF-β-inducible antagonist of TGF-β signaling and might participate in a negative feedback loop to control TGF-β signaling. In this study, the responsiveness of Smad7 to TGF-β1 was examined 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 exam the Smad7 and TGF-β1 expression abundance in BEP2D and BERP35T-2 at both transcription and translation level. Results: The expression level of Smad7 mRNA in BERP35T-2 cells was higher than that in BEP2D cells. When stimulated with TGF-β1, Smad7 expression was up-regulated evidently in BEP2D cells, but not significantly in BERP35T-2 cells. The abundance of TGF-β1 in the cytoplasm of BERP35T-2 was not significantly higher than in BEP2D (P>0.05); whereas the abundance of TGF-β1 in BERP35T-2 cell culture medium was significantly higher than in BEP2D cell culture medium (P<0.05). Conclusion: Over expression of Smad7 mRNA and down-regulation of the cells’ responsiveness to TGF-β1 in human lung cancer cell line might be involved in lung carcinogenisis.

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Correspondence to Zhang Kai-tai.

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Foundation item: This work was supported by the National “973” Key Basic Research Program of China (No. G1998051207).

Biography: HUO Yan-ying (1973–), female, candidate for doctor of medicine, Beijing Institute of Radiation Medicine, majors in molecular toxicology.

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Huo, Yy., Zhang, Kt., Li, By. et al. Responsiveness of Smad7 gene to TGF-β1 in the tumorigenesis. Chin. J. Cancer Res. 14, 170–174 (2002). https://doi.org/10.1007/s11670-002-0038-z

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  • DOI: https://doi.org/10.1007/s11670-002-0038-z

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