| 舒尼替尼诱导耐药鼻咽癌CNE2/DDP细胞表达NKG2DLs的机制 |
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| 引用本文： | 黄宇贤,王 杨,李玉华,杨玉莲,赵同峰,何庆梅,卢惠芳,贺艳杰,黄 睿,郭坤元.舒尼替尼诱导耐药鼻咽癌CNE2/DDP细胞表达NKG2DLs的机制[J].中国肿瘤生物治疗杂志,2010,17(3):256-261. |
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| 作者姓名： | 黄宇贤 王 杨 李玉华 杨玉莲 赵同峰 何庆梅 卢惠芳 贺艳杰 黄 睿 郭坤元 |
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| 作者单位： | 1. 南方医科大学,珠江医院,血液科,广东,广州,510282
2. 广东省人民医院,肺癌研究所,广东,广州,510080 |
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| 基金项目： | 国家自然科学基金资助项目（No. 30973454）；广东省自然科学基金重点项目（No. 9251051501000007） |
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| 摘 要： | 目的：初步探讨舒尼替尼诱导高、低表达ABCG2(ATPbinding cassette superfamily G member 2)分子的耐药鼻咽癌CNE2/DDP细胞（简称ABCG2highCNE2/DDP细胞、ABCG2lowCNE2/DDP细胞）中NKG2D配体（natural killer group 2 member D ligands，NKG2DLs）表达的分子机制。方法：Caspase8活化试剂盒和线粒体膜电位法分别检测NK细胞处理后ABCG2highCNE2/DDP细胞和ABCG2lowCNE2/DDP细胞caspase8活化水平和线粒体膜电位。RTPCR检测舒尼替尼处理前后两种CNE2/DDP细胞DNA损伤修复系统相关信号分子mRNA的表达。结果：CNE2/DDP细胞+NK细胞组中两种CNE2/DDP细胞caspase8活性均明显增强；舒尼替尼处理后的ABCG2low CNE2/DDP细胞+NK细胞组和ABCG2highCNE2/DDP细胞＋NK细胞组中caspase8的活性是处理前的2～2.5倍（P<0.01）。舒尼替尼预处理后，CNE2/DDP细胞和NK细胞共培养体系中两种CNE2/DDP细胞的线粒体膜电位分别为(76.58±2.32)%和(73.11±1.93)%，较舒尼替尼处理前明显降低（P<0.05）。舒尼替尼可上调两种CNE2/DDP细胞中ATR、CHK1和CHK2 mRNA的表达，并诱导P53和NFκB mRNA的表达。结论：舒尼替尼可能通过激活DNA损伤修复系统相关信号分子和NFκB的表达，诱导耐药鼻咽癌CNE2/DDP细胞NKG2DLs的表达，同时经由死亡受体信号通路和线粒体信号通路增强NK细胞诱导的肿瘤细胞凋亡。
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| 关 键 词： | 舒尼替尼 鼻咽肿瘤 NKG2D配体 自然杀伤细胞 DNA损伤 |
| 收稿时间： | 2009/12/12 0:00:00 |
| 修稿时间： | 2010/1/20 0:00:00 |
Mechanism of sunitinib inducing NKG2DLs expressions in multidrug resistant nasopharyngeal carcinoma CNE2/DDP cells |
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| HUANG Yu-xian,WANG Yang,LI Yu-hu,YANG Yu-lian,ZHAO Tong-feng,HE Qing-mei,LU Hui-fang,HE Yan-Jie,HUANG Rui and GUO Kun-yuan.Mechanism of sunitinib inducing NKG2DLs expressions in multidrug resistant nasopharyngeal carcinoma CNE2/DDP cells[J].Chinese Journal of Cancer Biotherapy,2010,17(3):256-261. |
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| Authors: | HUANG Yu-xian WANG Yang LI Yu-hu YANG Yu-lian ZHAO Tong-feng HE Qing-mei LU Hui-fang HE Yan-Jie HUANG Rui and GUO Kun-yuan |
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| Institution: | Department of Hematology, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, Guangdong, China;Lung Cancer Institute, Guangdong General Hospital, Guangzhou 510080, Guangdong, China;Department of Hematology, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, Guangdong, China;Department of Hematology, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, Guangdong, China;Department of Hematology, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, Guangdong, China;Department of Hematology, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, Guangdong, China;Department of Hematology, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, Guangdong, China;Department of Hematology, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, Guangdong, China;Department of Hematology, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, Guangdong, China;Department of Hematology, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, Guangdong, China |
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| Abstract: | Objective To investigate the mechanism by which unitinib induces up-regulation of NKG2D ligands(NKG2DLs) expressions in nasopharyngeal carcinoma CNE2/DDP cells with high or low ABCG2 expression(ABCG2highCNE2/DDP cells or ABCG2lowCNE2/DDP cells).Methods: Caspase-8 activity and mitochondrial membrane potential were detected by caspase-8 activity kit and mitochondrial membrane potential assay kit in ABCG2highCNE2/DDP cells or ABCG2lowCNE2/DDP cells after co-cultured with NK cells.Expressions of signal molecule... |
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| Keywords: | sunitinib nasopharyngeal neoplasms natural killer groups 2 member D ligand(NKG2DL) natural killer cell DNA damage |
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