基础医学与临床 ›› 2017, Vol. 37 ›› Issue (9): 1286-1291.

• 研究论文 • 上一篇    下一篇

CNTN-1促进人食管癌EC9706细胞侵袭和迁移

曹燕飞,任睿,罗向晖,杨晔,王水利   

  1. 陕西省人民医院
  • 收稿日期:2016-08-29 修回日期:2016-11-03 出版日期:2017-09-05 发布日期:2017-08-28
  • 通讯作者: 任睿 E-mail:weihuawh@yeah.net

CNTN-1 promotes the invasion and migration of human esophageal cancer cell line EC9706

  • Received:2016-08-29 Revised:2016-11-03 Online:2017-09-05 Published:2017-08-28

摘要: 目的 探讨接触蛋白-1(CNTN-1)在食管癌转移中的作用。方法 qPCR和Western blot法检测食管癌细胞系EC9706中CNTN-1的表达;RNA干扰和CNTN-1过表达质粒转染调整EC9706细胞CNTN-1的表达,并将细胞分为空白对照组、scrambled siRNA组、CNTN-1 siRNA组、pcDNA3.1-vector组、pcDNA3.1-CNTN-1组;BrdU和Transwell实验分别检测EC9706细胞增殖、侵袭和迁移能力;qPCR和Western blot检测基质金属蛋白酶MMP-2和MMP-9的表达。结果 CNTN-1在食管癌细胞EC9706中mRNA和蛋白水平较与正常食管上皮细胞显著上调(P<0.05);转染CNTN-1 siRNA后,EC9706细胞CNTN-1表达水平显著降低(P<0.05),细胞增殖、侵袭和迁移能力显著下降(P<0.05),同时细胞中侵袭转移相关蛋白MMP-2和MMP-9表达明显下降(P<0.05);CNTN-1过表达质粒转染细胞后,EC9706细胞内CNTN-1表达水平上调( P<0.05),细胞增殖、迁移和侵袭能力显著升高,同时MMP-2和MMP-9表达明显升高(P<0.05)。结论 CNTN-1可能通过调节MMP-2和MMP-9表达促进食管癌细胞的侵袭转移。

关键词: 食管癌, CNTN-1, 侵袭, 迁移

Abstract: Objective To investigate the effects of CNTN-1 on the invasion and migration of human esophageal cancer EC9706 cells and the possible mechanism. Methods The expression of CNTN-1 in human esophageal cancer EC9706 cells was measured by qPCR and Western blot. After transfection with CNTN-1 siRNA or CNTN-1, the cells were divided into control group, scrambled siRNA group, CNTN-1 siRNA group, pcDNA3.1-vector group and pcDNA3.1-CNTN-1 group. Cell proliferation, invasion and migration were respectively analyzed by BrdU assay and Transwell test. The expression of MMP-2 and MMP-9 were detected by qPCR and Western blot. Results The mRNA and protein expression of CNTN-1 were significantly upregulated in EC9706 cells. Compared with control, cell proliferation, invasion and migration, as well as the expression of MMP-2 and MMP-9 were significantly decreased by CNTN-1 siRNA, while they were increased by CNTN-1 overexpression (P<0.05). Conclusions CNTN-1 can influence the invasion and metastasis of esophageal cancer cells through the regulation of the expression of MMP-2 and MMP-9.