Background: Iodine-125 (125I) brachytherapy is an effective strategy for treating human tumors. The current study aimed to discover the mechanisms underlying the therapeutic action of 125I radiation in lung cancer, with a focus on its impact on the epithelial-mesenchymal transition (EMT). Materials and Methods: A549 cells, a human lung adenocarcinoma cell line, were treated with transforming growth factor β1 (TGF-β1) and/or 125I (control, TGF-β1, 125I, and TGF-β1 + 125I groups) to evaluate the effects of 125I on TGF-β1-induced EMT. After treatment, the viability of A549 cells was detected using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The expression of E-cadherin, N-cadherin, Vimentin, Smad3, and Snai1 markers and pathway molecules was measured. Results: 125I radiation inhibited the viability of A549 cells, both with and without TGF-β1 treatment. TGF-β1 intervention promoted the EMT of A549 cells, as demonstrated by the morphological transition from a polygonal shape to a spindle shape, reduced E-cadherin levels, and elevated Vimentin and N-cadherin expression. Notably, TGF-β1-activated EMT was significantly weakened by 125I radiation. Moreover, 125I radiation reversed TGF-β1-induced upregulation of Smad3 and Snai1 in A549 cells. Conclusion: 125I radiation suppresses the EMT by blocking TGF-β1/Smad3/Snai1 signaling, contributing to the treatment of lung cancer.
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