ERK信号通路参与赭曲霉毒素A诱导的人胃黏膜上皮细胞(GES-1)G2期阻滞的研究
ERK signaling pathway is involved in Ochratoxin A-induced G2 phase arrest in human gastric epithelium cells
目的：观察ERK信号通路在赭曲霉毒素A（OTA）诱导的人胃黏膜上皮细胞（GES-1）G2期阻滞中的作用，以期揭示OTA诱导G2期阻滞的可能分子机制。方法：不同浓度OTA（5、10、20 μM）处理GES-1细胞24小时，Western blot方法检测ERK的变化情况；给予ERK特异性阻断剂PD98059 (10 μM) 预处理细胞或采用siRNA干扰技术拮抗ERK信号通路，用流式细胞分析技术、Western blot方法、及免疫共沉淀技术检测细胞周期以及G2期调控因子（Cdc25C、Cdc2和CyclinB1）的变化情况。结果：OTA处理24h可以激活GES-1细胞内的ERK信号通路。ERK特异性阻断剂PD98059预处理及ERK siRNA转染可以拮抗OTA对GES-1细胞G2调控因子的下调作用。PD98059预处理及ERK siRNA转染可逆转OTA诱导的GES-1细胞G2期阻滞。结论：ERK信号通路通过调控G2期调控因子（Cdc25C、Cdc2和CyclinB1）的表达参与OTA诱导的GES-1细胞G2期阻滞。
Objecitve: To investigate the putative role of ERK signaling pathway in OTA-induced G2 arrest, and reveal the putative mechanisms of G2 arrest induced by OTA in human gastric epithelium cells in vitro. Methods: GES-1 cells were treated with different concentrations of OTA(5, 10 and 20 μM) for 24h, the effect of OTA on ERK was confirmed by Western blot. GES-1 cells were preincubated with PD98059 (10 μM) or reversely transfected with siRNA targeting ERK, then Western blot analysis, Flow cytometry and Immunoprecipitation were used to detect the distribution of cell cycle phases and the expression of G2 phase regulatory factors (Cdc25C、Cdc2 and CyclinB1). Results: Exposure of GES-1 cells to OTA at different concentrations of 5, 10 and 20 μM for 24 h could activate ERK signaling pathway. ERK specific inhibitor (PD98059) and ERK siRNA transfaction blocked the down-regulation of G2 phase regulatory factors (Cdc25C、Cdc2 and CyclinB1), and then abolished the G2 arrest induced by OTA. Conclusion: ERK signaling pathway was involved in OTA-induced G2 arrest in GES-1 cells by modulating G2 phase related factors.
崔晋峰、王俊灵、王媛、邢凌霄、严霞、刘静、张祥宏
基础医学分子生物学细胞生物学
赭曲霉毒素A胃黏膜上皮细胞G2期阻滞ERK信号转导通路
Ochratoxin Ahuman gastric epithelium cellsG2 arrestERK signaling pathway
崔晋峰,王俊灵,王媛,邢凌霄,严霞,刘静,张祥宏.ERK信号通路参与赭曲霉毒素A诱导的人胃黏膜上皮细胞(GES-1)G2期阻滞的研究[EB/OL].(2012-08-13)[2025-08-02].http://www.paper.edu.cn/releasepaper/content/201208-83.点此复制
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