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Objective:The aim of the study was to investigate the effect of c-Jun N-terminal protein kinase(JNK) signaling pathway on influencing the sensitivity to radiotherapy of human nasopharyngeal carcinoma CNE cells.Methods:Human nasopharyngeal carcinoma CNE multicellular spheroids(MCS) were constructed with three dimensional cell culture methods.Western blot was employed to analyze the activity of JNK signaling pathway in MCS after X-ray irradiation,and the expression of caspase-3 protein before and after using SP600125(a special inhibitor of JNK).X-ray induced cell apoptosis in MCS before and after treated with SP600125 were detected by TUNEL.Results:The level of JNK phosphorylation in MCS was a dynamic course after radiation,and there was a phosphorylation peaks at 2 h later,the apoptotic rate of MCS(P < 0.05) and the expression of caspase-3 protein(P < 0.05) were significantly increased after treated with SP600125.Conclusion:The transient activation of JNK played a important role in sensitivity to radiotherapy of CNE MCS via mediating survival signals,blocking this pathway accelerate cell apoptosis,which may be related to the increased expression of caspase-3.
Objective: The aim of the study was to investigate the effect of c-Jun N-terminal protein kinase (JNK) signaling pathway on influencing the sensitivity to radiotherapy of human nasopharyngeal carcinoma CNE cells. Methods: Human nasopharyngeal carcinoma CNE multicellular spheroids (MCS) were constructed with three dimensional cell culture methods. Western blot was employed to analyze the activity of JNK signaling pathway in MCS after X-ray irradiation, and the expression of caspase-3 protein before and after using SP600125 (a special inhibitor of JNK). X-ray induced cell apoptosis in MCS before and after treated with SP600125 were detected by TUNEL. Results: The level of JNK phosphorylation in MCS was a dynamic course after radiation, and there was a phosphorylation peaks at 2 h later, the apoptotic rate of MCS (P <0.05) and the expression of caspase-3 protein (P <0.05) were significantly increased after treated with SP600125.Conclusion: The transient activation of JNK played a significant role in sens itivity to radiotherapy of CNE MCS via mediating survival signals, blocking this pathway accelerate cell apoptosis, which may be related to the increased expression of caspase-3.