生物技术通报 ›› 2015, Vol. 31 ›› Issue (10): 242-248.doi: 10.13560/j.cnki.biotech.bull.1985.2015.10.035

• 研究报告 • 上一篇    下一篇

ERK1/2在食管鳞状细胞癌中促进细胞增殖、抑制凋亡及其调控机制的研究

刘凤霞,刘文娟,李建勇,陈胜国   

  1. 新疆医科大学人体解剖学教研室, 乌鲁木齐 830011
  • 收稿日期:2015-03-16 出版日期:2015-10-28 发布日期:2015-10-28
  • 作者简介:刘凤霞, 女, 博士, 副教授, 研究方向:消化道肿瘤; E-mail:liufengxia555@126.com
  • 基金资助:
    新疆医科大学校内支撑学科项目(XYDXK50780307)

A Study on the Regulation Mechanism of ERK1/2 Promoting Proliferation and Inhibiting Apoptosis in Esophageal Squamous Carcinoma

Liu Fengxia, Liu Wenjuan, Li Jianyong, Chen Shenguo   

  1. Department of Anatomy, College of Basic Medicine, Xinjiang University of Medical Science, Urumqi 830011
  • Received:2015-03-16 Published:2015-10-28 Online:2015-10-28

摘要: 探讨ERK1/2 在食管鳞状细胞癌(ESCC)中对肿瘤细胞增殖、凋亡的调控及其机制。平板克隆、细胞凋亡和细胞周期实验结果发现ERK1/2 MAPK通路抑制可减弱Eca109细胞克隆形成和增殖, 促进细胞凋亡, 减慢细胞周期; 进一步发现ERK1/2 MAPK通路抑制可以反转由miR-21过表达诱导的Eca109细胞增殖、凋亡和周期的变化; qRT-PCR和Western-blot免疫印迹结果发现ERK1/2 MAPK信号通路抑制可以下调内源性miR-21表达和反转外源性miR-21诱导的ERK1/2 MAPK信号通路活化。实验结果提示ERK1/2 MAPK通路抑制可能通过下调Eca109细胞中miR-21表达阻碍Eca109细胞增殖、促进细胞凋亡和减慢细胞周期, 最终导致ESCC细胞生长抑制。

关键词: 食管鳞状细胞癌(ESCC), ERK1/2 MAPK, Eca 109细胞增殖, 细胞凋亡, miR-21 

Abstract: This study aims to explore the role of ERK1/2 MAPK in the regulation mechanism of cell proliferation and apoptosis concerning of esophageal squamous carcinoma(ESCC). The results of plate colony, cell apoptosis and cycle revealed that the inhibition of ERK1/2 MAPK pathway eliminated the clone formation and proliferation of Eca109 cells, promoted cell apoptosis, and slowed down cell cycle; in addition, the inhibition of ERK1/2 MAPK pathway reversed the changes of proliferation, apoptosis and cycle induced by miR-21 overexpression. The results of qRT-PCR and Western blot showed that the inhibition of ERK1/2 MAPK pathway downregulated endogenous miR-21 expression, and also reversed the activation of ERK1/2 MAPK signal pathway induced by exogenous miR-21. The findings demonstrated that the inhibition of ERK1/2 MAPK pathway hindered Eca109 cell proliferation, promoted cell apoptosis, and retarded cell cycle via downregulation of miR-21 expression in Eca109 cell.

Key words: esophageal squamous cell carcinoma(ESCC), ERK1/2 MAPK, Eca 109 cell proliferation, cell apoptosis, miR-21