没食子酸通过活化线粒体通路诱导CNE-2鼻咽癌移植瘤细胞的凋亡
| 作者: |
1吴艳林,
1蔡政,
2张明智,
2付晓瑞
1 南阳市中心医院肿瘤科，河南 南阳 473000 2 郑州大学第一附属医院肿瘤科，郑州 450052 |
| 通讯: |
张明智
Email: mingzhi_zhang@126.com |
| DOI: | 10.3978/j.issn.2095-6959.2017.06.008 |
| 基金: | 河南省教育厅科学技术研究重点资助项目, 13A320413 |
摘要
目的：观察不同浓度的没食子酸(gallic acid，GA)对鼻咽癌移植荷瘤裸鼠的影响，并探讨其可能的作用机制。方法：建立人鼻咽癌CNE-2细胞株荷瘤裸鼠移植性肿瘤模型，随机分为6组：正常对照组(control，con组)，模型组(nasopharynx cancer，NPC组)，没食子酸10，20，40 μg/kg组(GA-10 μg/kg，GA-20 μg/kg，GA-40 μg/kg)和阳性对照组(顺铂，DDP组)；经相应处理后，处死裸鼠，测量瘤体积，称量瘤体重量并计算抑瘤率；流式细胞术检测肿瘤细胞的凋亡率；Western印迹检测肿瘤细胞中cytochrome C(Cyt C)、cleaved-cas 9，cleaved-cas 3与cleaved-PARP的蛋白表达水平。结果：与NPC组相比，给予GA后瘤体体积与重量随其浓度升高而减小，抑瘤率与肿瘤细胞凋亡率增大；与NPC组相比，肿瘤细胞线粒体中Cyt C的蛋白表达随GA浓度增加而减少，胞质中Cyt C的蛋白表达则相反，细胞中cleaved-cas 9，cleaved-cas 3与cleaved-PARP的蛋白水平显著增加，与GA浓度呈正相关。结论：没食子酸可能通过调控线粒体通路诱导鼻咽癌移植瘤细胞的凋亡。
关键词：
没食子酸
鼻咽癌瘤
抑瘤率
Caspase
线粒体通路
Gallic acid induced CNE-2 cell apoptosis on xenograft model in nude mice through mitochondria-dependent pathway
CorrespondingAuthor: ZHANG Mingzhi Email: mingzhi_zhang@126.com
DOI: 10.3978/j.issn.2095-6959.2017.06.008
Abstract
Objective: To investigate the effects of gallic acid (GA) on the xenograft model of nasopharynx cancer in nude mice and to study its possible mechanism. Methods: Xenograft model of human nasopharynx cancer was established by transplantation of human nasopharynx cancer cell CNE-2. The mice were divided into 6 groups: the control group, the nasopharynx cancer group, the galllic acid (10 μg/kg) group, the galllic acid (20 μg/kg) group, the galllic acid (40 μg/kg) group and the DDP group. The tumor dimensions and volume were measured and the tumor inhibiting rate was calculated. The apoptotic rate of CNE-2 cells was examined with flow cytometry. The protein levels of cytochrome C, cleaved-cas 9, cleaved-cas 3 and cleaved-PARP were detected by Western blotting. Results: Compared with the nasopharynx cancer group, the tumor volume and weight significantly decreased in the galllic acid group, and the inhibitory rate and apoptotic rate of the tumor dose-dependently increased. Moreover, galllic acid enhanced the release of cytochrome C from mitochondria to cytoplasm, leading to increase the protein levels of cleaved-cas 9, cleaved-cas 3 and cleaved-PARP. Conclusion: Galllic acid induces apoptosis of nasopharynx cancer cell CNE-2 through mitochondria-dependent pathway.