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mi R-21过表达诱导的Eca109细胞增殖、凋亡和周期的变化;q RT-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mi R-21表达和反转外源性mi R-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mi R-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。
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 mi R-21 overexpression. The results of q RT-PCR and Western blot showed that the inhibition of ERK1/2 MAPK pathway downregulated endogenous mi R-21 expression, and also reversed the activation of ERK1/2 MAPK signal pathway induced by exogenous mi R-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 mi R-21 expression in Eca109 cell.
出处
《生物技术通报》
CAS
CSCD
北大核心
2015年第10期242-248,共7页
Biotechnology Bulletin
基金
新疆医科大学校内支撑学科项目(XYDXK50780307)
