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目的研究花生四烯酸(AA)对鼻咽癌细胞增殖的影响及其潜在的分子机制。方法采用CCK-8法检测AA对鼻咽癌细胞系C666-1增殖的影响,以及雷帕霉素(rapamycin,Rap)、PP242与AA共同作用对C666-1细胞增殖的影响。同时采用免疫印迹法检测AA对鼻咽癌C666-1细胞哺乳动物雷帕霉素靶蛋白(mTOR)信号通路活性的影响,包括下游相关蛋白S6、Akt的表达水平及磷酸化水平,以及mTOR通路抑制剂Rap、PP242与AA共同作用对mTOR信号通路的影响。结果 AA可强烈促进C666-1细胞的增殖,mTOR通路抑制剂Rap、PP242均可抑制AA促进C666-1细胞增殖。AA可激活C666-1细胞mTORC1/2下游相关蛋白S6、Akt,使其磷酸化水平升高。mTORC1通路抑制剂Rap可阻断AA对mTORC1的激活,从而降低S6(S235/236)的磷酸化水平,mTORC1/2通路抑制剂PP242可阻断AA对mTORC1/2的激活,从而降低S6(S235/236)和Akt(S473)的磷酸化水平。结论花生四烯酸通过激活mTORC1/2信号通路促进鼻咽癌C666-1细胞系的增殖。
Objective To study the effects of arachidonic acid (AA) on the proliferation of nasopharyngeal carcinoma cells and its potential molecular mechanisms. Methods CCK-8 method was used to detect the effect of AA on the proliferation of C666-1 cell line and the effect of rapamycin (Rap), PP242 and AA on the proliferation of C666-1 cells. At the same time, the effect of AA on mammalian target of rapamycin (mTOR) signaling pathway, including the expression and phosphorylation of downstream proteins S6 and Akt, and the mTOR pathway Effects of Inhibitors Rap, PP242 and AA on mTOR Signaling Pathway. Results AA could strongly promote the proliferation of C666-1 cells. Both mTOR pathway inhibitors Rap and PP242 could inhibit the proliferation of C666-1 cells. AA can activate S6, Akt of mTORC1 / 2 downstream cells in C666-1 cells to increase its phosphorylation. The mTORC1 pathway inhibitor Rap can block the activation of mTORC1 by AA and thus the phosphorylation of S6 (S235 / 236). The mTORC1 / 2 pathway inhibitor PP242 can block the activation of mTORC1 / 2 by AA, / 236) and Akt (S473). Conclusion Arachidonic acid can promote the proliferation of C666-1 cell line by activating the mTORC1 / 2 signaling pathway.