阿克替苷通过调控ERK1/2信号通路抑制肝癌细胞上皮间质转化

袁倩倩; 何昱静; 温雪; 张久聪; 郑英; 卢利霞; 李斌; 于晓辉

doi:10.3971/j.issn.1000-8578.2023.22.0535

阿克替苷通过调控ERK1/2信号通路抑制肝癌细胞上皮间质转化

Acteoside Inhibits Epithelial Mesenchymal Transformation of Hepatoma Cells Through Regulation of ERK1/2 Signaling Pathway

摘要

摘要:
目的探讨阿克替苷（ACT）通过调控ERK1/2通路抑制人肝癌HCCLM3细胞上皮间质转化（EMT）的作用及其机制。
方法 CCK-8法检测肝癌细胞的增殖能力；划痕实验和Transwell实验检测肝癌细胞侵袭及迁移能力；实时定量PCR和蛋白质印迹实验检测ACT对ERK1/2信号通路和上皮间质转化相关基因（E-cadherin、N-cadherin）mRNA和蛋白的表达。
结果 CCK-8法检测结果显示，ACT可降低肝癌HCCLM3细胞的活性，抑制肝癌细胞的增殖能力，并与药物浓度和时间有一定的相关性。划痕实验和Transwell实验结果显示，ACT能抑制肝癌HCCLM3细胞迁移和侵袭能力，并呈浓度依赖性。荧光定量PCR和蛋白质印迹实验表明，ACT可下调ERK1/2信号通路相关基因mRNA和蛋白的表达，上调EMT相关基因E-cadherin mRNA和蛋白的表达，下调N-cadherin mRNA和蛋白的表达。
结论 ACT可抑制人肝癌HCCLM3细胞EMT、侵袭及迁移，其作用机制与下调ERK1/2信号通路密切相关。

Abstract:
Objective To investigate the effect and mechanism of acteoside (ACT) in inhibiting epithelial-mesenchymal transition (EMT) in human hepatoma HCCLM3 cells by regulating the ERK1/2 pathway.
Methods CCK-8 assay was used to detect the effect of hepatocellular carcinoma cell proliferation. The invasion and migration of HCC cells were detected by scratch and Transwell tests. The mRNA and protein expression levels of the ERK1/2 signaling pathway and EMT-related genes (E-cadherin and N-cadherin) were detected by real-time PCR and Western blot analyses.
Results ACT reduced the activity of HCCLM3 cells and inhibited the proliferation of HCC cells, and the effects had certain correlation with drug concentration and time. ACT inhibited the migration and invasion process of HCCLM3 cells in a concentration-dependent manner. ACT downregulated the mRNA and protein expression of genes related to the ERK1/2 signaling pathway. It increased the mRNA and protein expression levels of the EMT-related gene E-cadherin but decreased those of N-cadherin.
Conclusion ACT could inhibit EMT and the invasion and migration of HCCLM3 cells in human hepatoma, and the underlying mechanism is closely related to the downregulation of the ERK1/2 signaling pathway.

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