Yana He1, Liang Li2, Jihua Liu3, Xuening Zhang4. 1. Department of Medical Imaging, Second Hospital of Tianjin Medical University, Tianjin, China; Department of Medical Imaging, The First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, China. 2. Department of Medical Imaging, Second Hospital of Tianjin Medical University, Tianjin, China. 3. Department of Medical Imaging, The First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, China. 4. Department of Medical Imaging, Second Hospital of Tianjin Medical University, Tianjin, China. Electronic address: zhangxn2266@163.com.
Abstract
PURPOSE: Metastatic non-small cell lung cancer (NSCLC) has posed a great clinical challenge with high mortality. Iodine-125 (I-125) seed brachytherapy has not been widely applied in clinic against NSCLC. METHODS AND MATERIALS: Mice were injected with human H23 NSCLC cells to establish a mouse xenograft model, which received I-125 seed implantation. The curative effect, pathological impairments, and survival rate of mice were investigated. Changes in the expression levels of epithelial-mesenchymal transition (EMT) markers, including N-cadherin, E-cadherin, and vimentin, in the xenograft tumors were analyzed using reverse transcription polymerase chain reaction and Western blot. RESULTS: The tumor volume and pathological effect were reduced by I-125 seed implant. I-125 seed implant also significantly improved survival rate of the model mice. Expression patterns of N-cadherin, E-cadherin, and vimentin were reversed in I-125 seed-implanted mice in comparison with control mice, indicating suppressed EMT. CONCLUSIONS: I-125 seed brachytherapy significantly inhibits NSCLC by suppressing EMT in a mouse model.
PURPOSE: Metastatic non-small cell lung cancer (NSCLC) has posed a great clinical challenge with high mortality. Iodine-125 (I-125) seed brachytherapy has not been widely applied in clinic against NSCLC. METHODS AND MATERIALS: Mice were injected with human H23 NSCLC cells to establish a mouse xenograft model, which received I-125 seed implantation. The curative effect, pathological impairments, and survival rate of mice were investigated. Changes in the expression levels of epithelial-mesenchymal transition (EMT) markers, including N-cadherin, E-cadherin, and vimentin, in the xenograft tumors were analyzed using reverse transcription polymerase chain reaction and Western blot. RESULTS: The tumor volume and pathological effect were reduced by I-125 seed implant. I-125 seed implant also significantly improved survival rate of the model mice. Expression patterns of N-cadherin, E-cadherin, and vimentin were reversed in I-125 seed-implanted mice in comparison with control mice, indicating suppressed EMT. CONCLUSIONS: I-125 seed brachytherapy significantly inhibits NSCLC by suppressing EMT in a mouse model.