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腺苷单磷酸活化蛋白激酶的激活通过上皮-间充质转化靶向 Claudin-1 抑制舌鳞状细胞癌细胞的迁移。

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.

机构信息

Department of Basic Medicine, Hubei University of Chinese Medicine, Wuhan, China.

Hubei Shizhen Laboratory, Wuhan, Hubei, China.

出版信息

Animal Model Exp Med. 2024 Oct;7(5):606-616. doi: 10.1002/ame2.12444. Epub 2024 Jul 17.

DOI:10.1002/ame2.12444
PMID:39017036
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11528389/
Abstract

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.

CONCLUSIONS

Our results indicated that AMPK activation suppresses TSCC cell migration by targeting Claudin-1 and EMT pathways.

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，特别是其对细胞迁移的影响。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

36 例 TSCC 组织标本进行 Claudin-1 免疫组织化学染色。通过 Western blot 和免疫荧光分析评估 Claudin-1 在 TSCC 细胞中的表达和分布。使用短发夹 RNA 转染建立 Claudin-1 敲低细胞系。通过划痕愈合实验评估迁移效应。此外，通过 Western blot 测量 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。单磷酸腺苷激活的蛋白激酶（AMPK）的激活导致 Claudin-1 的表达增加和膜转位，抑制 TSCC 细胞迁移和上皮-间充质转化（EMT）。相反，Claudin-1 的敲低逆转了 AMPK 激活对迁移和 EMT 抑制作用。

结论

我们的结果表明，AMPK 激活通过靶向 Claudin-1 和 EMT 通路抑制 TSCC 细胞迁移。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a1d/11528389/0592826d570a/AME2-7-606-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a1d/11528389/2fc5d7101970/AME2-7-606-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a1d/11528389/5da3a04c1fc9/AME2-7-606-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a1d/11528389/51fbd36a91a7/AME2-7-606-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a1d/11528389/299bed18ed4d/AME2-7-606-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a1d/11528389/b380073f77f7/AME2-7-606-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a1d/11528389/0592826d570a/AME2-7-606-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a1d/11528389/2fc5d7101970/AME2-7-606-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a1d/11528389/5da3a04c1fc9/AME2-7-606-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a1d/11528389/51fbd36a91a7/AME2-7-606-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a1d/11528389/299bed18ed4d/AME2-7-606-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a1d/11528389/b380073f77f7/AME2-7-606-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a1d/11528389/0592826d570a/AME2-7-606-g001.jpg

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