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Updated: Jul 5, 2025

Induction and Analysis of Epithelial to Mesenchymal Transition

Induction and Analysis of Epithelial to Mesenchymal Transition

Published on: August 27, 2013

一个部分上皮层-介质细胞过渡签名,用于高侵略性结直肠癌细胞,在营养限制下生存

Gil A Pastorino¹, Ilir Sheraj², Kerstin Huebner¹

¹Institute of Pathology, Universitätsklinikum Erlangen, Friedrich-Alexander Universität Erlangen-Nürnberg, Erlangen, Germany.

The Journal of pathology

|January 18, 2024

概括

饥饿诱导结肠直肠癌细胞的部分上皮-介质细胞过渡 (p-EMT),增加迁移和化学抵抗. 一种新的三重基因特征 (SERPINE1,SOX10,EGFR) 预示着这些侵袭性癌细胞的预后不佳.

科学领域:

在瘤学瘤学.
细胞生物学细胞生物学
分子生物学分子生物学

背景情况:

部分上皮层-介质细胞过渡 (p-EMT) 是一种与癌细胞迁移,转移和化学抵抗相关的混合细胞状态.
营养压力,如饥饿,可以影响癌细胞的可塑性和行为.
在营养压力下了解p-EMT机制对于开发新的癌症疗法至关重要.

研究的目的:

在饥饿条件下研究p-EMT在结直肠癌 (CRC) 细胞中的诱导.
为了确定一个p-EMT基因签名,可以预测CRC患者的预后.
阐明饥饿诱导的p-EMT背后的分子机制及其治疗影响.

主要方法:

饥饿诱导的p-EMT在CRC细胞系 (HCT116,DLD1,HT29) 和体内 (chorioallantoic膜模型) 的功能性表征.
特定于EMT的定量聚合酶连锁反应 (qPCR) 阵列用于基因查和in silico基因签名建立.
高分辨率的免疫光成像分析表皮生长因子受体 (EGFR) 表达和局部化.

主要成果:

饥饿诱导了CRC细胞中的p-EMT,改变了增殖,形态和药物敏感性.
发现了一种新型的三重基因特征 (SERPINE1,SOX10,EGFR),与CRC患者 (CMS4亚型) 无病生存率差相关.
饥饿诱导的p-EMT增加了迁移潜力和化学抵抗,与E-cadherin处理和内化相关,可通过MG132逆转.

结论:

饥饿会触发CRC细胞中的p-EMT机制,这与转移期间的营养压力瘤细胞有关.
鉴定到的三重基因特征和E-cadherin变异具有预后价值和潜在的治疗点.
针对这种饥饿诱导的p-EMT过程可能会抑制瘤细胞的扩散并克服耐药性.

关键词:

在E-cadherin加工过程中.欧洲农村基金内部化共识分子亚型4共识分子亚型4 中级的EMT是中间的EMT.一部分的EMT.预后预后预后蛋白质酶体蛋白质组是什么饥饿饥饿饥饿饥饿饥饿

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