title: [Regulation of Smad7 gene by TGF-beta 1 in process of malignant transformation].
abstract: OBJECTIVE
  Escape from transforming growth factor-beta(TGF-beta)-induced inhibition of growth and proliferation may contribute to tumorigenesis. Smad7 is inhibitory Smads of TGF-beta s signal transduction pathway and prevents TGF-beta signaling. The disorder of Smad7 may lead to the perturbation of TGF-beta signal pathway. In this study, The authors analyzed the expression of Smad7 mRNA and the regulation of Smad7 gene by TGF-beta 1 in the process of malignant transformation of BEP2D cells to investigate the mechanism of cells malignant transformation.
  
  
  METHODS
  Cells were cultured and stimulated with TGF-beta 1 followed by RNA extraction. Purified total RNA from TGF-beta 1 treated cells and untreated controls and performed an expression analysis with a human Smad7-specific probe applying Northern blot. As a loading control for the Northern experiment, the membrane was hybridized with a human glyceraldehyde-3-phosphate dehydrogenase(GAPDH) probe. Proteins were extracted from BEP2D and BERP35T-2 cells, then perform Western blot to examine the expression level of TGF-beta 1.
  
  
  RESULTS
  Before stimulation with TGF-beta 1, the expression level of Smad7 in the BERP35T-2 cells were higher than that in the BEP2D cells. When stimulated with TGF-beta 1, Smad7 expression levels was upregulated evidently in BEP2D cells, but not significant in BERP35T-2 cells. The expression level of endogenetic TGF-beta 1, BERP35T-2 cells was a little higher than BEP2D cells.
  
  
  CONCLUSIONS
  Over expression of Smad7 mRNA and down-regulation of the cells' responsiveness to TGF-beta 1 in human lung cancer cell line which induced by alpha-particles should be one of the mechanism of radiation induced lung cancer.
authors.affiliation: Department of Molecular Toxicology, Beijing Institute of Radiation Medicine, Beijing 100850, P. R. China.
authors.forename: Yan-ying
authors.initials: YY
authors.lastname: Huo
authors.forename: Kai-tai
authors.initials: KT
authors.lastname: Zhang
authors.forename: Bang-yin
authors.initials: BY
authors.lastname: Li
authors.forename: Rui-feng
authors.initials: RF
authors.lastname: Duan
authors.forename: Bao-xing
authors.initials: BX
authors.lastname: Fan
authors.forename: Xiao-qiong
authors.initials: XQ
authors.lastname: Xiang
authors.forename: Ying-chun
authors.initials: YC
authors.lastname: Hu
authors.forename: Ling
authors.initials: L
authors.lastname: Xie
authors.forename: De-chang
authors.initials: DC
authors.lastname: Wu
mesh_terms: D015153:Blotting, Western; D002471:Cell Transformation, Neoplastic / Q000378:metabolism*; D002478:Cells, Cultured; D004268:DNA-Binding Proteins / Q000235:genetics*; D005786:Gene Expression Regulation / Q000187:drug effects*; D006801:Humans; D012333:RNA, Messenger / Q000032:analysis; D051906:Smad7 Protein; D015534:Trans-Activators / Q000235:genetics*; D016212:Transforming Growth Factor beta / Q000494:pharmacology*; D053773:Transforming Growth Factor beta1
chemical_list: D004268:DNA-Binding Proteins; D012333:RNA, Messenger; C497806:SMAD7 protein, human; D051906:Smad7 Protein; C508960:TGFB1 protein, human; D015534:Trans-Activators; D016212:Transforming Growth Factor beta; D053773:Transforming Growth Factor beta1