WNT7A promotes tumorigenesis of head and neck squamous cell carcinoma via activating FZD7/JAK1/STAT3 signaling.
10.1038/s41368-024-00279-y
- Author:
Qingling HUANG
1
;
Yi XIAO
2
;
Ting LAN
2
;
Youguang LU
2
;
Li HUANG
3
;
Dali ZHENG
4
Author Information
1. Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, China.
2. Fujian Key Laboratory of Oral Diseases, School and Hospital of Stomatology, Fujian Medical University, Fuzhou, China.
3. Department of Dentistry, The First Affiliated Hospital of Fujian Medical University, Fuzhou, China. lihuang@fjmu.edu.cn.
4. Fujian Key Laboratory of Oral Diseases, School and Hospital of Stomatology, Fujian Medical University, Fuzhou, China. dalizheng@fjmu.edu.cn.
- Publication Type:Journal Article
- MeSH:
Animals;
Humans;
Squamous Cell Carcinoma of Head and Neck;
Carcinogenesis/genetics*;
Cell Transformation, Neoplastic;
Wnt Signaling Pathway;
Disease Models, Animal;
Head and Neck Neoplasms/genetics*;
Wnt Proteins;
Frizzled Receptors/genetics*;
Janus Kinase 1;
STAT3 Transcription Factor
- From:
International Journal of Oral Science
2024;16(1):7-7
- CountryChina
- Language:English
-
Abstract:
Wnt signaling are critical pathway involved in organ development, tumorigenesis, and cancer progression. WNT7A, a member of the Wnt family, remains poorly understood in terms of its role and the underlying molecular mechanisms it entails in head and neck squamous cell carcinoma (HNSCC). According to the Cancer Genome Atlas (TCGA), transcriptome sequencing data of HNSCC, the expression level of WNT7A in tumors was found to be higher than in adjacent normal tissues, which was validated using Real-time RT-PCR and immunohistochemistry. Unexpectedly, overexpression of WNT7A did not activate the canonical Wnt-β-catenin pathway in HNSCC. Instead, our findings suggested that WNT7A potentially activated the FZD7/JAK1/STAT3 signaling pathway, leading to enhanced cell proliferation, self-renewal, and resistance to apoptosis. Furthermore, in a patient-derived xenograft (PDX) tumor model, high expression of WNT7A and phosphorylated STAT3 was observed, which positively correlated with tumor progression. These findings underscore the significance of WNT7A in HNSCC progression and propose the targeting of key molecules within the FZD7/JAK1/STAT3 pathway as a promising strategy for precise treatment of HNSCC.
