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论文摘要

口腔鳞癌细胞过表达MHC-Ⅰ类链相关蛋白A对自然杀伤细胞与细胞毒性T淋巴细胞杀伤活性影响的实验研究

Natural killer and cytotoxic T lymphocyte-mediated cytotoxicity enhanced by genetic overexpression of MHC class Ⅰ chain-related protein A in oral squamous cell carcinoma:An experimental study in vivo

作者:李超 石芳琼 杨丹 王洁 翦新春 蒋灿华

Author:Li Chao1, Shi Fangqiong1, Yang Dan1, Wang Jie2, Jian Xinchun1, Jiang Canhua1

收稿日期:2012-02-25          年卷(期)页码:2012,30(1):32-32-35

期刊名称:华西口腔医学杂志

Journal Name:West China Journal of Stomatology

关键字:口腔,鳞状细胞癌,MHC-Ⅰ类链相关蛋白A,杀伤活性,基因治疗,

Key words:oral,squamous cell carcinoma,MHC class Ⅰ chain-related protein A,cytotoxicity,gene therapy,

基金项目:

国家自然科学基金资助项目(30772437);湖南省科技计划一般基金资助项目(06sk3026,06sk3044)

中文摘要

目的探讨口腔鳞癌细胞过表达MHC-Ⅰ类链相关蛋白A(MICA)对自然杀伤细胞(NK)与细胞毒性T淋巴细胞(CTL)杀伤活性的影响。方法通过绘制细胞生长曲线、检测细胞周期、进行平板集落形成率及裸鼠皮下成瘤等方法对稳定转染并过表达MICA的口腔鳞癌细胞株进行生物学特性鉴定。采用乳酸脱氢酶释放法及流式细胞术分析口腔鳞癌细胞过表达MICA对NK与CTL细胞杀伤活性及自然杀伤细胞2族成员D(NKG2D)受体表达的影响。结果口腔鳞癌细胞转染MICA基因后主要生物学特性未发生改变,但能显著增强NK与CTL细胞杀伤活性并上调其表面NKG2D的表达,与未转染及转染空白载体的细胞比较,差异有统计学意义(P

英文摘要

Objective To investigate the effect on natural killer(NK) and cytotoxic T lymphocyte(CTL)-mediated cytotoxicity by genetic overexpression of MHC class Ⅰ chain-related protein A(MICA) in oral squamous cell carcinoma (OSCC). Methods The OSCC cells by genetic overexpression of MICA were detected to identify the biological features including cell growth curve, cell cycle distribution, plate clone forming rate and tumorigenicity in nude mice. The expression of natural killer group 2, member D(NKG2D) receptor and the cytotoxicity to target tumor cells of NK92 and CTL cells, which co-cultured with the transfected OSCC cells or the non-transfected or blank vector-transfected controls, were measured by flow cytometry and lactate dehydrogenase(LDH) release assay. Results There was no difference in biological features before and after MICA gene transfection to OSCC cells. Flow cytometry and LDH release assay showed that MICA-overexpressed OSCC cells enhanced the cytotoxicity to target tumor cells and up-regulated the expression of NKG2D on NK92 and CTL(P

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