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A Comprehensive Analysis of the Role of PAX9 in Head and Neck Squamous Cell Carcinoma.

Authors :
Zeng L
Yun W
Luo WL
Source :
Current molecular medicine [Curr Mol Med] 2025 Jan 15. Date of Electronic Publication: 2025 Jan 15.
Publication Year :
2025
Publisher :
Ahead of Print

Abstract

Background: Paired box 9 (PAX9) has been linked to several human disorders; however, its relevance in Head And Neck Squamous Cell Carcinoma (HNSCC) remains unknown.<br />Methods: The difference in PAX9 mRNA expression in pan-cancer was analyzed utilizing The Cancer Genome Atlas (TCGA), and the level of PAX9 protein expression across various types of cancer was assessed utilizing the Human Protein Atlas (HPA) and UALCAN databases, as well as the cellular localization of PAX9. UALCAN studied the methylation levels of PAX9 in pan-cancer. The predictive significance of PAX9 in pan-cancer was assessed utilizing the Kaplan-Meier Plotter website. Functional enrichment analysis was carried out with the "cluster Profiler" program. By employing CCK8 and colony formation methods, the influence of PAX9 on the growth of HNSCC cells was evaluated. By conducting a transwell experiment, we assessed the influence of PAX9 on the migration of HNSCC cells. Western blotting was used to determine the levels of Bax and Bcl-2, two proteins involved in the regulation of apoptosis. A nude mouse model was established to study the impact of PAX9 overexpression on the growth of subcutaneous HNSCC tumors.<br />Results: In HNSCC, the expression of PAX9 was found to be low, while levels of promoter methylation rose considerably. Low PAX9 expression has been linked to a decrease in overall survival (OS) rates among individuals with HNSCC. Furthermore, overexpressing the PAX9 gene decreased HNSCC cell proliferation, migration, and invasion while boosting apoptosis rates.<br />Conclusion: The abnormal expression of PAX9 is linked to various cancers. In HNSCC, PAX9 is a potential tumor suppressor, inhibiting tumor invasion and migration. The results reveal a potentially significant new therapeutic target for HNSCC.<br /> (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Details

Language :
English
ISSN :
1875-5666
Database :
MEDLINE
Journal :
Current molecular medicine
Publication Type :
Academic Journal
Accession number :
39819533
Full Text :
https://doi.org/10.2174/0115665240328109241205084841