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… Click to show full abstract
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.
               
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