KT活化参与EGF诱导胃癌BGC823细胞发生上皮-间质转化
KT activation is involved in epithelial-mesenchymal transition in gastric cancer BGC 823 cells
上皮-间质转化（EMT）能导致肿瘤细胞转移和耐药。本研究为明确AKT如何影响EGF诱导胃癌细胞发生EMT，倒置相差显微镜检测细胞形态，免疫印迹检测蛋白表达，Transwell法检测细胞迁移能力。EGF作用于胃癌BGC823细胞后，细胞形态发生EMT改变，E-cadherin蛋白表达减少，Vimentin蛋白表达增多，细胞迁移能力增强，同时AKT发生磷酸化。加入AKT磷酸化抑制剂LY294002后，AKT磷酸化被明显抑制，EGF诱导的EMT被逆转，细胞迁移能力减弱。
Epithelial-mesenchymal transition (EMT) leads to cancer metastasis and drug resistance. In order to clarify how AKT influences EGF-stimulated EMT in gastric cancer cells, cell morphology was recorded by inverted phase-contrast microscopy, protein expression was analyzed by western blot, cell migration was determined by transwell assay. After incubated with EGF, gastric cancer BGC823 cells underwent EMT, with downregulation of E-cadherin and upregulation of vimentin. Meanwhile, the migration capacity of BGC823 cells was increased. During this process, AKT was phosphorylated. Using AKT inhibitor LY294002, AKT phosphorylation was inhibited. Furthermore, EGF-induced EMT was reversed and EGF-stimulated migration was attenuated.
李贺明、曲秀娟、刘云鹏、赵雷、徐玲
基础医学肿瘤学细胞生物学
胃癌EGF上皮-间质转化KT
gastric cancerEGFEMTAKT
李贺明,曲秀娟,刘云鹏,赵雷,徐玲.KT活化参与EGF诱导胃癌BGC823细胞发生上皮-间质转化[EB/OL].(2014-11-17)[2025-05-29].http://www.paper.edu.cn/releasepaper/content/201411-302.点此复制
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