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

Author:

Zhou Xin‐Yue12ORCID,Liu Qiu‐Ming34,Li Zhuang1,Liu Xia‐Yang1,Zhao Qi‐Wei1,Wang Yu1ORCID,Wu Feng‐Hua12,Zhao Gang1,Sun Rui56,Guo Xiao‐Hong12

Affiliation:

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

2. Hubei Shizhen Laboratory Wuhan Hubei China

3. Sino‐German Biomedical Center Hubei University of Technology Wuhan China

4. Center of Applied Biotechnology Wuhan Institute of Bioengineering Wuhan China

5. Department of Stomatology, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital Third Hospital of Shanxi Medical University Taiyuan China

6. Department of Oral and Maxillofacial Surgery Shanxi Provincial People's Hospital Taiyuan China

Abstract

AbstractBackgroundThe 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.Methods36 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.ResultsClaudin‐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.ConclusionsOur results indicated that AMPK activation suppresses TSCC cell migration by targeting Claudin‐1 and EMT pathways.

Funder

National Natural Science Foundation of China

Publisher

Wiley

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