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.
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，特别是对细胞迁移的影响。在这里，本研究旨在探讨Claudin-1在TSCC细胞迁移中的作用及其机制.
方法：对36个TSCC组织样本进行Claudin-1的免疫组织化学染色。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。使用短发夹RNA转染建立Claudin-1敲低细胞系。通过伤口愈合试验评估迁移效果。此外，通过蛋白质印迹法测定EMT相关分子的表达.
结果：随着TSCC恶性程度的增加，Claudin-1表达降低。腺苷一磷酸活化蛋白激酶（AMPK）活化导致Claudin-1表达增加和膜转位，抑制TSCC细胞迁移和上皮间质转化（EMT）。相反，Claudin-1敲低逆转了这些由AMPK激活引起的对迁移和EMT的抑制作用。
结论：我们的结果表明，AMPK激活通过靶向Claudin-1和EMT途径抑制TSCC细胞迁移。
方法：对36个TSCC组织样本进行Claudin-1的免疫组织化学染色。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。使用短发夹RNA转染建立Claudin-1敲低细胞系。通过伤口愈合试验评估迁移效果。此外，通过蛋白质印迹法测定EMT相关分子的表达.
结果：随着TSCC恶性程度的增加，Claudin-1表达降低。腺苷一磷酸活化蛋白激酶（AMPK）活化导致Claudin-1表达增加和膜转位，抑制TSCC细胞迁移和上皮间质转化（EMT）。相反，Claudin-1敲低逆转了这些由AMPK激活引起的对迁移和EMT的抑制作用。
结论：我们的结果表明，AMPK激活通过靶向Claudin-1和EMT途径抑制TSCC细胞迁移。
