山楂酸通过PI3K/Akt/mTOR通路诱导鼻咽癌CNE2细胞自噬研究

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。

Maslinic acid induces autophagy through PI3K/Akt/mTOR pathway in human nasopharyngeal carcinoma cells

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-p110αand the phosphorylation of Akt and m TOR.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.