单磷酸腺苷激活蛋白激酶通过上皮-间质转化靶向Claudin-1抑制舌鳞状细胞癌细胞的迁移。

Q1 Health Professions

Animal models and experimental medicine Pub Date : 2024-07-17 DOI:10.1002/ame2.12444

Xin-Yue Zhou, Qiu-Ming Liu, Zhuang Li, Xia-Yang Liu, Qi-Wei Zhao, Yu Wang, Feng-Hua Wu, Gang Zhao, Rui Sun, Xiao-Hong Guo

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引用次数: 0

摘要

背景：Claudin-1在舌鳞状细胞癌（TSCC）转移中的作用需要进一步阐明，尤其是它对细胞迁移的影响。在此，我们的研究旨在探讨 Claudin-1 在 TSCC 细胞迁移中的作用及其潜在机制。方法：对36个TSCC组织样本进行Claudin-1免疫组化染色，并进行Western印迹和免疫荧光分析，以评估Claudin-1在TSCC细胞中的表达和分布。利用短发夹 RNA 转染技术建立了 Claudin-1 基因敲除细胞系。通过伤口愈合实验评估了迁移效应。此外，还通过 Western 印迹法测定了 EMT 相关分子的表达：结果：Claudin-1的表达随着TSCC恶性程度的增加而降低。单磷酸腺苷激活蛋白激酶（AMPK）的激活导致Claudin-1的表达和膜转运增加，抑制了TSCC细胞的迁移和上皮-间质转化（EMT）。相反，Claudin-1的敲除逆转了AMPK激活对迁移和EMT的抑制作用：我们的研究结果表明，AMPK活化可通过靶向Claudin-1和EMT通路抑制TSCC细胞迁移。

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The activation of adenosine monophosphate–activated protein kinase inhibits the migration of tongue squamous cell carcinoma cells by targeting Claudin-1 via epithelial–mesenchymal transition

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The activation of adenosine monophosphate–activated protein kinase inhibits the migration of tongue squamous cell carcinoma cells by targeting Claudin-1 via epithelial–mesenchymal transition

Background

The role of Claudin-1 in tongue squamous cell carcinoma (TSCC) metastasis needs further clarification, particularly its impact on cell migration. Herein, our study aims to investigate the role of Claudin-1 in TSCC cell migration and its underlying mechanisms.

Methods

36 TSCC tissue samples underwent immunohistochemical staining for Claudin-1. Western blotting and immunofluorescence analyses were conducted to evaluate Claudin-1 expression and distribution in TSCC cells. Claudin-1 knockdown cell lines were established using short hairpin RNA transfection. Migration effects were assessed through wound healing assays. Furthermore, the expression of EMT-associated molecules was measured via western blotting.

Results

Claudin-1 expression decreased as TSCC malignancy increased. Adenosine monophosphate–activated protein kinase (AMPK) activation led to increased Claudin-1 expression and membrane translocation, inhibiting TSCC cell migration and epithelial–mesenchymal transition (EMT). Conversely, Claudin-1 knockdown reversed these inhibitory effects on migration and EMT caused by AMPK activation.