Suppr超能文献

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.

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/11528389/2fc5d7101970/AME2-7-606-g003.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验