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目的:研究miR-124对鼻咽癌细胞株上皮间充质转化(epithelial-mesenchymal transitions,EMT)和放疗敏感性的影响。方法:转染miR-124 mimic或inhibitor入鼻咽癌细胞株,划痕实验检测miR-124对鼻咽癌EMT影响;细胞转染成功24 h后X线照射,检测细胞株中Caspase-3活性及凋亡细胞比例;Ed U方法检测放疗后细胞增殖能力;Western blot检测信号通路蛋白。结果:划痕实验结果显示miR-124能抑制鼻咽癌细胞株EMT。Caspase-3活性检测结果提示,miR-124过表达细胞株接受放疗后Caspase-3活性显著上升(P<0.01)。流式细胞仪结果显示,miR-124能增加细胞株放疗后凋亡。Ed U结果显示,miR-124能抑制放疗后细胞的增殖。Western blot结果表明过表达miR-124的细胞株接受放疗后,p-Akt含量显著下降。结论:miR-124可能通过Akt信号通路抑制鼻咽癌细胞株EMT,增加其放疗敏感性。这为鼻咽放疗增敏提供了新的可行的研究方向。
Objective: To investigate the effect of miR-124 on epithelial-mesenchymal transitions (EMT) and radiosensitivity in nasopharyngeal carcinoma cell lines. Methods: miR-124 mimic or inhibitor was transfected into nasopharyngeal carcinoma cell lines. Scratch assay was used to detect the effect of miR-124 on the EMT of NPC. 24 h after transfection, X-ray was used to detect the activity of Caspase-3 And the proportion of apoptotic cells; Ed U method to detect cell proliferation after radiotherapy; Western blot detection signal pathway protein. Results: Scratch test results showed that miR-124 can inhibit the nasopharyngeal carcinoma cell line EMT. The results of Caspase-3 activity test showed that the activity of Caspase-3 in miR-124 overexpression cell line was significantly increased after radiotherapy (P <0.01). Flow cytometry results show that miR-124 can increase cell apoptosis after radiotherapy. Ed U results show that miR-124 can inhibit the proliferation of cells after radiotherapy. Western blot results showed that miR-124-overexpressing cell lines treated with radiotherapy, p-Akt significantly decreased. Conclusion: miR-124 may inhibit the EMT of nasopharyngeal carcinoma cell line through Akt signaling pathway and increase its radiosensitivity. This provides a new feasible research direction for nasopharyngeal radiosensitization.