目的 研究山楂酸对鼻咽癌CNE2细胞增殖和自噬的影响，探讨PI3K/Akt/mTOR通路在该过程中的调控作用。方法 采用CCK-8法检测不同浓度的山楂酸作用不同时间对CNE2细胞增殖的影响；MDC染色法检测不同浓度山楂酸处理CNE2细胞24 h后自噬小体的形成情况；Western blotting法检测山楂酸对CNE2细胞自噬相关蛋白及PI3K/AKT/mTOR通路关键蛋白表达的影响。结果 与溶剂对照组相比，山楂酸可以抑制CNE2细胞的增殖，而且随药物处理时间和浓度的增加，抑制效果增强（P<0.05）；山楂酸能够诱导细胞自噬小体的形成，且可显著提高Atg5和LC3-II/LC3-I的表达，降低p62的表达；此外，山楂酸可抑制PI3K-p110α、p-Akt和p-mTOR的蛋白表达。结论 山楂酸可抑制鼻咽癌细胞增殖，诱导鼻咽癌细胞发生自噬，其机制与PI3K/Akt/mTOR信号通路有关，可作为治疗鼻咽癌的潜在药物研究。

Objective To investigate the effects of maslinic acid (MA) on the proliferation and autophagy in nasopharyngeal carcinoma CNE2 cells and to elucidate the regulatory role of PI3K/Akt/mTOR pathway in this process. Methods The effect of MA on the proliferation of CNE2 cells was assessed by CCK-8. MDC staining of autophagic vacuoles was performed for autophagy analysis. Additionally, the levels of autophagy-and PI3K/Akt/mTOR-associated proteins were examined using western blot analysis. Results MA significantly inhibited the proliferation of CNE2 cells in a dose-and time-dependent manner. MA displayed autophagy-inducing effect, as shown by the increased MDC-labeled vacuoles, up-regulated LC3-II/LC3-I ratio and Atg5, as well as the down-regulated p62 level after MA treatment. Moreover, we observed that MA inhibited the expression of PI3K-p110α and the phosphorylation of Akt and mTOR. Conclusion MA inhibits the proliferation and induces the autophagy of CNE2 cells, the mechanism may be related to the PI3K/Akt/mTOR signaling pathway. These results imply that MA may be a potential anti-cancer agent for use in the treatment of nasopharyngeal carcinoma.

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国家自然科学基金资助项目（81874408）；湖南省自然科学基金项目（2017JJ3246）；湖南省自然科学基金项目（2016JJ6117）；湖南中医药大学基础医学学科基金；湖南省教育厅优秀青年基金（19B439）