索拉非尼对食管癌EC9706细胞的生长抑制作用

熊羽; 樊青霞; 赵国强

doi:10.3971/j.issn.1000-8578.2015.04.002

索拉非尼对食管癌EC9706细胞的生长抑制作用

1. 450052 郑州，郑州大学附属第一医院肿瘤科；2. 450001 郑州，郑州大学基础医学院微生物免疫研究室

详细信息

作者简介:
熊羽（1988-），女，硕士在读，主要从事恶性肿瘤的基础研究和临床治疗工作

通讯作者:
樊青霞，E-mail:fqx2246@126.com

中图分类号: R735.1
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出版历程
- 收稿日期: 2014-04-20
- 修回日期: 2014-07-21
- 刊出日期: 2015-04-24

Inhibitory Effect of Sorafenib on Growth of Human Esophageal Cancer Cells EC9706

1. Department of Oncology, The First Hospital Affiliated to Zhengzhou University, Zhengzhou 450052, China; 2. Department of Microbiology and Immunology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou 450001, China

摘要

摘要: 目的探讨索拉非尼（sorafenib）体外对EC9706细胞生长抑制作用及其机制。方法 qRTPCR检测sorafenib作用后MMP-2、MMP-9、TIMP1、AKT和Bcl-2 mRNA的表达；Western blot检测sorafenib作用后AKT、p-AKT、Bcl-2、MMP-2和TIMP1蛋白表达水平的变化；Hoechst/PI 染色荧光显微镜观察sorafenib诱导的细胞凋亡/坏死；细胞划痕实验观察sorafenib对EC9706细胞的迁移抑制作用。结果与对照组相比，qRT-PCR显示sorafenib下调MMP-2、MMP-9、AKT、Bcl-2 mRNA表达，上调TIMP1 mRNA 表达（P<0.05）；Western blot显示sorafenib降低MMP-2、AKT、p-AKT、Bcl-2蛋白的表达水平，上调TIMP1蛋白表达水平（P<0.05）；荧光显微镜观察发现sorafenib诱导红染细胞增加（P<0.05）；细胞划痕实验发现sorafenib作用后划痕明显变宽，并且具有浓度依赖性（P<0.05）。结论索拉非尼能够上调TIMP1表达水平、下调MMP-2、MMP-9、AKT、Bcl-2表达水平，可以抑制食管鳞癌EC9706细胞的迁移、促进凋亡坏死，这些可能是其产生抗肿瘤作用的机制之一。
- 索拉非尼 /
- EC9706细胞 /
- 细胞生长抑制 /
- MMP-2/MMP-9/TIMP1 /
- AKT/Bcl-2
Abstract: Objective To investigate the inhibitory effect of sorafenib on the growth of esophageal cancer cells EC9706 in vitro and its mechanism. Methods Effect of sorafenib on the expression of MMP-2, MMP-9, TIMP1, AKT and Bcl-2 were detected by qRT-PCR. Effect of sorafenib on the expression of AKT, p-AKT, Bcl-2, MMP-2 and TIMP1 were detected by Western blot. Cell apoptosis/necrosis induced by sorafenib were observed by Hoechst/PI staining. The inhibitory effect of sorafenib on EC9706 cells migration was observed by cell scratch test. Results qRT-PCR data showed downregulation of MMP-2, MMP-9, AKT, Bcl-2 and upregulation of TIMP1 mRNA, compared with the control group(P<0.05); furthermore, Western blot analysis revealed the expression of MMP-2, AKT, p-AKT, Bcl-2 proteins were downregulated and TIMP1 protein expression was upregulated in the sorafenib groups compared with the control group(P<0.05).Sorafenib was found not only to inhibit the migration of EC9706 cells in vitro by cell scratch test, but also to promote cells apoptosis in vitro by Hoechst/PI apoptosis/necrosis detection(P<0.05). Conclusion Sorafenib could upregulate the expression of TIMP1, downregulate the expression of MMP-9, AKT, MMP-2 and Bcl-2,and inhibit the migration and promote apoptosis/necrosis of esophageal cancer cells EC9706. These may be its anticancer mechanism.
- Sorafenib /
- EC9706 /
- Cell growth inhibition /
- MMP-2/MMP-9/TIMP1 /
- AKT/Bcl-2