Mechanism Of Radioactive ¹²⁵I Particles On EMT Of Lung Adenocarcinoma Cells

Objective（s）:To study the inhibitory effect of radioactive ¹²⁵I particles on the proliferation of lung adenocarcinoma A549 cells and explore the mechanism of radioactive ¹²⁵I particles inhibiting the epithelial-mesenchymal phenotype transformation of A549 cells.Methods:The experiment was divided into four groups:A549 cell group;A549cells+TGF-β1 factor group;A549 cells+¹²⁵I particle group;A549 cells+TGF-β1factor+¹²⁵I particle group,in which TGF-β1 was used as inducer to induce epithelial-mesenchymal phenotype transformation of lung adenocarcinoma A549 cells.The cell survival and growth of the four groups were detected by MTT assay.Western blot and RT-PCR were used to detect the expression changes of E-cadherin,N-cadherin,Smad3,Vimentin and Snai1 proteins and genes in the four groups respectively.Results:MTT results showed that radioactive ¹²⁵I particles could inhibit the growth of lung adenocarcinoma A549 cells.Western blot and RT-PCR results showed that TGF-β1 induced epithelial-mesenchymal phenotype transformation of lung adenocarcinoma A549 cells,and the protein and gene expression of E-cadherin decreased（P<0.05）,while the protein and gene expression of N-cadherin,vimentin and snai1 increased（P<0.05）,and the protein and gene expression of Smad3increased（P<0.05）.Radioactive ¹²⁵I particles inhibited the generation of EMT in lung adenocarcinoma A549 cells,and the protein and gene expression of E-cadherin increased（P<0.05）,while the protein and gene expression of N-cadherin,vimentin and snai1 decreased（P<0.05）,and the protein and gene expression of pathway molecule Smad3 decreased（P<0.05）.The signal pathway of radioactive ¹²⁵I particles inhibiting epithelial-mesenchymal phenotype transformation of lung adenocarcinoma A549 cells is TGF-β/Smad pathway.Conclusion（s）:Radioactive ¹²⁵I particles can inhibit the proliferation of A549lung adenocarcinoma cells.TGF-β1 factor induces epithelial-mesenchymal phenotype transformation of lung adenocarcinoma A549 cells,while radioactive ¹²⁵I particles inhibit epithelial-mesenchymal phenotype transformation of lung adenocarcinoma A549 cells by up-regulating E-cadherin and down-regulating N-cadherin,vimentin and snai1.Radioactive ¹²⁵I particles inhibit epithelial-mesenchymal phenotype transformation of lung adenocarcinoma A549 cells by inhibiting TGF-β/Smad.