阿司匹林对同源不同辐射抗拒能力鼻咽癌细胞的凋亡诱导作用

发布时间：2018-03-21 11:54

本文选题：鼻咽癌　切入点：辐射抗拒性　出处：《中国病理生理杂志》2017年11期 　论文类型：期刊论文

【摘要】：目的:探讨阿司匹林诱导同源不同辐射抗拒能力鼻咽癌细胞株CNE2R/CNE2凋亡的作用及其机制。方法:采用MTT法、流式细胞术和Western blot法检测并比较阿司匹林对CNE2R和CNE2细胞活力、细胞凋亡及凋亡相关蛋白procaspase-3、cleaved caspase-3、procaspase-9、procaspase-12、PARP、cleaved PARP、Bcl-2和Bax,以及PI3K p110α、Akt和p27蛋白水平的影响。结果:阿司匹林抑制同源不同辐射抗拒能力细胞CNE2R/CNE2的活力(阿司匹林对CNE2细胞作用24、48和72 h的IC50分别为6.18、3.92和3.06 mmol/L,对CNE2R细胞作用24、48和72 h的IC50分别为7.05、3.90和2.20 mmol/L,两者差异无统计学显著性)。阿司匹林作用48 h后,CNE2R细胞凋亡率升高,明显高于CNE2细胞(P0.05)。阿司匹林作用48 h后,CNE2和CNE2R细胞中procaspase-3、procaspase-9、procaspase-12和PARP的蛋白水平降低,cleaved caspase-3和cleaved PARP的蛋白水平升高(P0.05);PI3K p110α和Akt蛋白水平下降,Bcl-2水平降低,Bax水平升高,Bcl-2/Bax比值降低,p27水平升高(P0.05)。结论:阿司匹林对同源不同辐射抗拒能力鼻咽癌细胞株CNE2R和CNE2具有同等细胞活力抑制作用;并且可以诱导细胞凋亡,且对抗辐射细胞株CNE2R的凋亡诱导作用更明显。阿司匹林的抗癌作用可能与其影响PI3K/Akt信号通路及其下游蛋白的水平有关。
[Abstract]:Objective: to investigate the effect of aspirin on apoptosis of nasopharyngeal carcinoma cell line CNE2R/CNE2 with different radioresistance and its mechanism. Methods: MTT assay, flow cytometry and Western blot assay were used to detect and compare the activity of aspirin on CNE2R and CNE2 cells. Apoptosis and apoptosis-related protein procaspase-3 / cleaved caspase-3 / caspase-3 / caspase-9 / proccaspase-12 / parapsid cleaved the levels of Bcl-2 and Bax, as well as the protein levels of PI3K p110 伪 -Akt and p27. Results: aspirin inhibited the activity of CNE2R/CNE2 in cells with different radioresistance (Aspirin acted on CNE2 cells for 2448 and 72 h). The IC50 of CNE2R cells treated for 24 h and 72 h were 7.05 渭 mol / L and 2.20 mmol / L, respectively. There was no significant difference between the two groups. The apoptosis rate of CNE2R cells increased after 48 h of aspirin treatment. The protein levels of procaspase-3, procaspase-9, procaspase-12 and PARP in CNE2 cells were significantly higher than those in CNE2 cells treated for 48 h. The protein levels of procaspase-9, procaspase-12 and cleaved PARP decreased in caspase-3 and cleaved PARP. The protein levels of P0.05 PI3K p110 伪 and Akt decreased the level of Bcl-2 and the ratio of Bcl-2 / Bax increased. Conclusion: aspirin has the same inhibitory effect on the viability of nasopharyngeal carcinoma cell lines CNE2R and CNE2 with different radioresistance. The anticancer effect of aspirin may be related to its influence on the level of PI3K/Akt signaling pathway and its downstream protein.
【作者单位】：中山大学中山医学院病理生理教研室;
【基金】：国家自然科学基金资助项目(No.81372410) 广东省科技计划(No.2013B031800002;No.2015A020211006)
【分类号】：R739.63

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