口腔医学研究 ›› 2015, Vol. 31 ›› Issue (7): 653-657.

• 基础研究论著 • 上一篇    下一篇

过表达IL-18诱导舌鳞癌细胞凋亡机制的初步研究

郭宇1,侯旭1,李正强1,李佳1,徐志民1,岳丽伟2,刘炜炜1*   

  1. 1. 吉林大学口腔医院颌面外科 吉林 长春 130021;
    2. 吉林省伊通县人民医院
  • 收稿日期:2014-12-29 出版日期:2015-07-28 发布日期:2015-07-28
  • 通讯作者: 刘炜炜,E-mail:33962344@qq.com
  • 作者简介:郭宇(1993~ ),男,回族,河南人,硕士在读,主要从事口腔肿瘤基因治疗的基础研究。
  • 基金资助:
    吉林省科技发展计划-青年科研基金项目(编号:20150520040JH);吉林省卫生计生青年科研课题(编号:2014Q019);吉林省教育厅"十二五"科学技术研究规划项目(编号:440020031111);吉林大学白求恩医学科研支持计划-青年科研基金项目(编号:2013208063)

Preliminary Study on Apoptosis Mechanism of Tongue Squamous Cell Carcinoma Cells Induced by Overexpressed -IL-18

GUO Yu, HOU Xu, LI Zheng-qiang, et al   

  1. School of Stomatology, Jilin University,Changchun 130021
  • Received:2014-12-29 Online:2015-07-28 Published:2015-07-28

摘要: 目的:探究白介素18(IL-18)的过表达对舌鳞癌细胞活性和凋亡的影响。方法:构建稳定转染人IL-18cDNA的舌鳞癌CRL1623细胞系,免疫荧光、qPCR和Western Blot证实IL-18的过表达;流式细胞术、吉姆萨染色和MTT法检测转染后CRL1623细胞活性的改变;qPCR检测凋亡相关基因的表达;用稳转的CRL1623细胞建立舌鳞癌细胞裸鼠移植瘤模型,体内观察IL-18过表达对移植瘤生长的影响。结果:过表达的IL-18可以诱导CRL1623细胞凋亡。与对照组相比,实验组IL-18的表达量上调,caspase 3、7和9的表达量增加并被活化,IFN-γ和细胞色素C的mRNA表达量上调。与对照组裸鼠相比,实验组裸鼠移植瘤的生长受到了抑制(P<0.05)。结论:IL-18能够通过启动经典的凋亡途径诱导舌鳞癌细胞凋亡。

关键词: 白介素18, 舌鳞状细胞癌, 基因表达, 细胞凋亡, 移植瘤模型

Abstract: Objective:To investigate the effects of IL-18 overexpression on cell viability and apoptosis of tongue squamous cell carcinoma cells in vitro and in vivo. Methods: Human IL-18 cDNA was stably transfected into CRL1623 cells,which was confirmed by immunofluorescence, quantitative reverse transcription-PCR (q-PCR) and Western Blot. Flow cytometry, Giemsa staining and MTT assay were performed to detect changes of cell viability. q-PCR was performed to detect alteration of the expression of apoptosis-related genes. IL18-stably-transfected CRl1623 cells were incubated subcutaneously into BALB/c-nu mice to establish xenografted model to observe the effect of IL-18 overexpression on xenografted tumor growth in vivo. Results: The overexpression of IL-18 reduced TSCC cell viability via inducing cell apoptosis. Compared with CRL1623-Vec cells, IL-18 expression activated caspase 3, 7, and 9 via inducing their cleavage and increased the expression of interferon (IFN)-γ and cytochrome C mRNA expression in CRL1623-IL18 cells. Compared with control group(incubated with CRL1623-Vec),the tumor growth of experimental group(incubated with CRL1623-IL18) was obviously inhibited(P<0.05). Conclusion: The IL-18 protein can induce apoptosis of CRL1623 via initiating the intrinsic apoptosis pathway.

Key words: IL-18, Tongue squamous cell carcinoma, Gene expression, Cell apoptosis, Xenografted model

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