Knockdown of Nav1.5 inhibits cell proliferation, migration and invasion via Wnt/β-catenin signaling pathway in oral squamous cell carcinoma. (13th May 2020)

• Record Type: Journal Article
• Authors: Xu, Xiaoli; Dai, Yongzheng; Feng, Linfei; Zhang, Hongli; Hu, Yukun; Xu, Le; Zhu, Xinwei; Jiang, Yong
• Is Part Of: Acta biochimica et biophysica Sinica. Volume 52:Number 5(2020)
• Page Start: 527
• Page End: 535
• Publication Date: 2020-05-13
• Subjects: oral squamous cell carcinoma (OSCC) -- Nav1.5 -- Wnt/β-catenin signaling pathway; Biochemistry -- Periodicals; Biophysics -- Periodicals; 572.05
• DOI: 10.1093/abbs/gmaa021
• Languages: English
• ISSNs: 1672-9145

Abstract

Abstract: Oral squamous cell carcinoma (OSCC) is a common type of malignant oral cancer that has a high recurrence rate. Voltage-gated sodium channel Nav1.5 was reported to be highly up-regulated in various types of cancers. However, the regulatory mechanism of Nav1.5 in cancers including OSCC still remains elusive. In this study, Nav1.5 was found to be highly expressed in OSCC tissues and cells. Through the analysis of clinical characteristics of patients, we found that the expression level of Nav1.5 was closely related to neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio, tumor-node-metastasis stage, and lymph node metastasis. Moreover, we found that Nav1.5 mainly located on the cell membrane as well as cytoplasm and knockdown of Nav1.5 promoted cell apoptosis and decreased proliferation in OSCC. Transwell assay results showed that knockdown of Nav1.5 effectively suppressed the migration and invasion in OSCC. In addition, knockdown of Nav1.5 was found to inhibit the protein and mRNA expression levels of β-catenin, cyclin D1, and c-Myc in the Wnt/ β - catenin signaling pathway. In summary, these results indicated that Nav1.5 may be involved in the progression of OSCC through the Wnt/β -catenin signaling pathway.