食管癌是我国常见的消化系统恶性肿瘤，其中食管鳞状细胞癌（ESCC）占所有食管癌病例的90%。目前主要的治疗方法是手术切除联合术后放疗。在本研究中，我们使用两种ESCC细胞系来确定氧化苦参碱（OMT）是否抑制ESCC，其机制是否涉及MEK1/ERK/β-catenin通路，以及OMT如何调节该通路以影响ESCC的发生发展。通过细胞计数试剂盒-8 (CCK-8) 检测以及克隆形成、迁移和侵袭、伤口愈合、Hoechst 33258 和蛋白质印迹分析来监测 OMT 治疗的效果。还通过分子对接和细胞稳定性实验评估了OMT与靶标之间的关系。这些发现表明OMT可能抑制ESCC的发展和转移，并且OMT通过ERK/β-catenin/EMT通路靶向MEK1来抑制ESCC细胞的迁移和侵袭。此外，体内研究证实OMT可以抑制NOG小鼠ESCC细胞系的生长，而不会对其他器官造成损害。总之，体外实验表明，OMT 通过抑制 ERK/β-catenin/EMT 通路，从而靶向 ESCC 中的 MAP2K1 (MEK1)，从而阻止 ESCC 细胞的迁移和侵袭。版权所有 © 2024 Elsevier B.V. 保留所有权利。

Esophageal, cancer is a prevalent malignant tumour of the digestive system in China, and esophageal squamous cell carcinoma (ESCC) accounts for 90 % of all esophageal cancer cases. Currently, the primary treatment involves surgical resection combined with postoperative radiotherapy. In this study, we used two ESCC cell lines to determine whether oxymatrine (OMT) inhibits ESCC, whether the mechanism involves the MEK1/ERK/β-catenin pathway, and how OMT modulates this pathway to affect the development of ESCC. The effects of OMT treatment were monitored with Cell Counting Kit-8 (CCK-8) assays as well as with clony formation, migration and invasion, wound healing, Hoechst 33258, and Western blot analyses. The relationship between OMT and the target was also evaluated by molecular docking and cell stability experiments. These findings suggest that ESCC development and metastasis may be inhibited by OMT and that OMT targets MEK1 through the ERK/β-catenin/EMT pathway to suppress ESCC cell migration and invasion. In addition, in vivo studies confirmed that OMT can inhibit the growth of ESCC cell lines in NOG mice without causing damage to other organs. In conclusion, in vitro experiments, revealed that OMT prevents the migration and invasiveness of ESCC cells by inhibiting the ERK/β-catenin/EMT pathway and thus targeting MAP2K1 (MEK1) in ESCC.Copyright © 2024 Elsevier B.V. All rights reserved.