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Correlation of signal transducer and activator of transcription-3 and β-catenin expression in laryngeal squamous cell carcinoma

OBJECTIVE: The specific roles of phosphorylated signal transducer and activator of transcription-3 (p-STAT3) and β-Catenin in laryngeal squamous cell carcinoma (LSCC) remain unclear. METHODS: In this study, the correlations between p-STAT3, β-Catenin, and clinicopathological characteristics were inv...

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Detalles Bibliográficos
Autores principales: Sun, Yajing, Lu, Xiuying, Li, Hui, Li, Xiaoming
Formato: Online Artículo Texto
Lenguaje:English
Publicado: SAGE Publications 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10107985/
https://www.ncbi.nlm.nih.gov/pubmed/37032609
http://dx.doi.org/10.1177/03000605231166228
Descripción
Sumario:OBJECTIVE: The specific roles of phosphorylated signal transducer and activator of transcription-3 (p-STAT3) and β-Catenin in laryngeal squamous cell carcinoma (LSCC) remain unclear. METHODS: In this study, the correlations between p-STAT3, β-Catenin, and clinicopathological characteristics were investigated using tissues and clinical data from 124 LSCC cases. Immunohistochemistry and immunofluorescence assays were used to examine p-STAT3 and β-Catenin expression and localization in these samples. Kaplan–Meier survival and Cox regression analyses were performed to evaluate the prognostic significance of these proteins. LSCC cell lines were treated with a STAT3 inhibitor (dihydroartemisinin) or activator (interleukin-6) to explore the mechanism of p-STAT3 and β-Catenin. RESULTS: There was an inverse correlation between p-STAT3 and β-Catenin expression in the LSCC samples. Patients with high p-STAT3 and low β-Catenin expression levels had significantly worse overall survival. Multivariate Cox regression analysis revealed that lymph node metastasis and β-Catenin expression were both independently correlated with unfavorable overall survival. Cell treatment with the p-STAT3 inhibitor inhibited the nuclear accumulation of β-Catenin, while p-STAT3 activator treatment could promote β-Catenin translocation to the nucleus. CONCLUSION: Overall, our data indicate that p-STAT3 expression is associated with LSCC by promoting β-Catenin degradation.