Expression and prognostic value of mothers against decapentaplegic homolog 7 in head and neck squamous cell carcinoma.
10.7518/hxkq.2025.2024341
- Author:
Haihui ZHAO
1
;
Xiaojuan ZHONG
2
;
Yi HUANG
2
;
Wei FEI
1
Author Information
1. School of Stomatology, Southwest Medical University, Luzhou 646000, China.
2. Oral Medicine Center, Sichuan Provincial Academy of Medical Sciences & Sichuan Provincial People's Hospital, Chengdu 610072, China.
- Publication Type:Journal Article
- Keywords:
diagnosis;
head and neck squamous cell carcinoma;
immunotherapy;
mothers against decapentaplegic homolog 7;
vascular cell adhesion molecule 1
- MeSH:
Humans;
Smad7 Protein/metabolism*;
Prognosis;
Squamous Cell Carcinoma of Head and Neck;
Head and Neck Neoplasms/pathology*;
Cell Line, Tumor;
Cell Movement;
Cell Proliferation;
Signal Transduction;
Gene Expression Regulation, Neoplastic;
Gene Silencing;
Computational Biology
- From:
West China Journal of Stomatology
2025;43(5):660-670
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVES:This study aimed to explore the biological functions and clinical value of mothers against decapentaplegic homolog (SMAD) 7 in head and neck squamous cell carcinoma (HNSCC) through bioinformatics analysis and basic experiments.
METHODS:The expression of SMAD7 in HNSCC in public databases was studied. Western blot was used to detect the expression of SMAD7 in HNSCC cell lines and normal epithelial cells. The SMAD7 highly expressed HNSCC cell line HSC-4 was silenced, and CCK-8, Transwell assays, and cell scratch experiments were conducted to study the effect of SMAD7 on the biological functions of HSC-4 cells. HNSCC expression profile data were obtained from UCSC xena, and genes related to SMAD7 were selected for gene ontology and Kyoto encyclopedia of genes and genomes gene enrichment analysis, construction of a co-expression gene interaction network, and screening of related cell signaling pathways. Western blot was used to detect the expression changes of proteins in the related cell signaling pathways in HNSCC cells with silenced SMAD7. cBioPortal was utilized to analyze the mutation rate of the SMAD7 gene, and the MethSurv database was used to analyze the methylation level of the SMAD7 gene and its correlation with prognosis. The receiver operating characteristic curve was used to assess the diagnostic value of SMAD7 for HNSCC. TIMER2.0 was used to analyze the correlation between SMAD7 expression and immune cell infiltration.
RESULTS:SMAD7 was highly expressed in HNSCC tumor tissues and some cell lines. Silencing the expression of SMAD7 can significantly inhibit the proliferation, migration, and invasion of cancer cells. Silencing SMAD7 can induce the downregulation of vascular cell adhesion molecule 1 (VCAM-1). The bioinformatics analysis showed that the mutation rate of the SMAD7 gene and the methylation level were significantly correlated with the prognosis of patients with HNSCC. The expression of SMAD7 was related to the level of immune cell infiltration in HNSCC.
CONCLUSIONS:SMAD7 promotes the proliferation, migration, and invasion of HNSCC cells by regulating the expression of VCAM-1. It may be a potential tumor biomarker and therapeutic target for HNSCC.
