Radiotherapy induces cell cycle arrest and cell apoptosis in nasopharyngeal carcinoma via the ATM and Smad pathways
| Autor: | Lu He, Liu Jinquan, Ming-Yi Li, Meng-Yao Wang, Ling Lin, Dong-Ping Chen, Yi Yu, Wen-Jin Yin, Bin Qi, Li Zhouyu |
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| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Cancer Research CDC25A Cell cycle checkpoint Cell Survival medicine.medical_treatment Fluorescent Antibody Technique Apoptosis Smad Proteins Ataxia Telangiectasia Mutated Proteins SMAD Histones Transforming Growth Factor beta1 Mice 03 medical and health sciences 0302 clinical medicine In vivo medicine Animals Humans Phosphorylation Cell Proliferation Pharmacology Nasopharyngeal Carcinoma Radiotherapy business.industry Carcinoma Nasopharyngeal Neoplasms Cell Cycle Checkpoints Cell cycle medicine.disease Cell biology Radiation therapy Disease Models Animal 030104 developmental biology Oncology Nasopharyngeal carcinoma 030220 oncology & carcinogenesis Heterografts Molecular Medicine business Signal Transduction Research Paper |
| Zdroj: | Cancer Biology & Therapy. 18:681-693 |
| ISSN: | 1555-8576 1538-4047 |
| Popis: | Nasopharyngeal carcinoma (NPC) is a common malignant neoplasm of the head and neck which is harmful to human's health. Radiotherapy is commonly used in the treatment of NPC and it induces immediate cell cycle arrest and cell apoptosis. However, the mechanism remains unknown. Evidences suggested the activation of Ataxia telangiectasia mutated (ATM) pathway and Smad pathway are 2 of the important crucial mediators in the function of radiotherapy. In this study, we performed in vitro assays with human nasopharyngeal carcinoma CNE-2 cells and in vivo assays with nude mice to investigate the role of the ATM and Smad pathways in the treatment of nasopharyngeal carcinoma with radiotherapy. The results suggested that radiation induced activation of ATM pathway by inducing expression of p-ATM, p-CHK1, p-CHK2, p15 and inhibiting expression of p-Smad3. In addition, Caspase3 expression was increased while CDC25A was decreased, leading to cell cycle arrest and cell apoptosis. On the other hand, activation of Smad3 can inhibited the ATM pathway and attenuated the efficacy of radiation. In summary, we suggest that both ATM and Smad pathways contribute to the cell cycle arrest and cell apoptosis during nasopharyngeal carcinoma cells treated with radiation. |
| Databáze: | OpenAIRE |
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