相关实验视频
Updated: Jun 17, 2025

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Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
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由IL-1β激活的PI3K/AKT和MEK/ERK通路协调促进部分上皮层-介质细胞过渡的诱导
Yosuke Tabei1, Yoshihiro Nakajima2
1Health and Medical Research Institute, National Institute of Advanced Industrial Science and Technology (AIST), 2217-14 Hayashi-Cho, Takamatsu, Kagawa, 761-0395, Japan. y-tabei@aist.go.jp.
Cell communication and signaling : CCS
|August 8, 2024
概括
介质素-1β (IL-1β) 通过PI3K/AKT和MEK/ERK通路诱导部分上皮质-介质酶过渡 (EMT). 针对这两种途径可以预防纤维化和转移.
科学领域:
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
- 在瘤学瘤学.
背景情况:
- 表皮-介质细胞过渡 (EMT) 对于发育,伤口愈合,纤维化和癌症转移至关重要.
- 介质素-1β (IL-1β) 是已知的EMT诱导剂,但其精确的信号机制尚不清楚.
- 了解IL-1β在EMT中的作用对于开发针对相关疾病的疗法至关重要.
研究的目的:
- 阐明IL-1β诱导的部分EMT所涉及的特定信号传导途径.
- 研究PI3K/AKT和MEK/ERK通路在IL-1β介导的EMT中的作用.
- 通过针对这些途径来探索潜在的治疗策略.
主要方法:
- 使用了人类肺上皮层A549细胞.
- 用IL-1β刺激细胞,并评估部分EMT标记物 (维门丁,E-cadherin).
- 使用PI3K抑制剂 (LY294002) 和MEK/ERK抑制剂 (FR180204) 来阻止特定的途径.
- 分析了表皮生长因子受体 (EGFR) 和IL-1受体 (IL-1R) 途径的下游信号事件.
主要成果:
- IL-1β诱导了部分EMT表型,其特征是增加了维门和迁移潜力,而没有完全失去E-cadherin.
- PI3K/AKT通路的抑制显著抑制了IL-1β介导的部分EMT.
- 抑制MEK/ERK通路也显著减少了IL-1β诱导的部分EMT.
- 两种PI3K/AKT和MEK/ERK通路分别在EGFR和IL-1R的下游被激活.
结论:
- 通过PI3K/AKT和MEK/ERK信号通路的协调作用,IL-1β触发了部分EMT.
- 这些途径分别在EGFR和IL-1R的下游被激活.
- 同时抑制PI3K/AKT和MEK/ERK通路对于治疗纤维化和转移等部分EMT相关疾病具有前途.
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