Pathology, research and practice · 2025
SCEL expression in tumor tissues: A potential prognostic biomarker for recurrent papillary thyroid carcinoma.
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Lin Zexin, Xiao Yingsheng, Wu Lin
Аннотация
BACKGROUND: Although papillary thyroid carcinoma (PTC) generally has a favorable prognosis, recurrence occurs in a significant number of patients, and its underlying mechanisms remain incompletely understood. This study investigated the prognostic significance of SCEL expression in recurrent PTC.
METHODS: SCEL expression was analyzed in PTC and normal tissues using GEPIA and TIMER2.0 databases, with validation by immunohistochemistry (IHC) in clinical samples. SCEL levels were compared between recurrent PTC (n = 50), non-recurrent PTC (n = 150), and tissues using Mann-Whitney U tests. Associations with clinicopathological features were assessed. Kaplan-Meier (log-rank) and Cox regression analyses evaluated survival outcomes. Relationships between SCEL, epithelial-mesenchymal transition (EMT), and immune cell infiltration were investigated using TIMER2.0, IHC, and correlation analysis.
RESULTS: Significantly elevated SCEL expression in PTC tissues versus normal controls (P < 0.01). Higher SCEL levels in recurrent PTC versus non-recurrent PTC (P < 0.01), correlating with increased recurrence risk. SCEL expression levels were significantly correlated with TNM stage, AJCC stage, and I-131 treatment status (P < 0.01). Lower SCEL expression predicted significantly improved prognosis in recurrent PTC patients. Multivariate Cox analysis confirmed low SCEL as an independent protective factor for disease-free survival (DFS) (HR = 0.358, 95 % CI: 0.149-0.861, P = 0.022). Recurrence showed no significant association with EMT pathways. This prognostic advantage was mechanistically linked to enhanced tumor immune cell infiltration in the low-SCEL group (P < 0.01), whereas high SCEL correlated with an immunosuppressive microenvironment.
CONCLUSIONS: This study identifies SCEL as a recurrence-associated potential biomarker in PTC. Critically, lower SCEL expression may serve as a potential independent protective factor, predicting improved DFS in recurrent PTC patients. This survival benefit is mediated through modulation of the tumor immune microenvironment rather than EMT pathways.
METHODS: SCEL expression was analyzed in PTC and normal tissues using GEPIA and TIMER2.0 databases, with validation by immunohistochemistry (IHC) in clinical samples. SCEL levels were compared between recurrent PTC (n = 50), non-recurrent PTC (n = 150), and tissues using Mann-Whitney U tests. Associations with clinicopathological features were assessed. Kaplan-Meier (log-rank) and Cox regression analyses evaluated survival outcomes. Relationships between SCEL, epithelial-mesenchymal transition (EMT), and immune cell infiltration were investigated using TIMER2.0, IHC, and correlation analysis.
RESULTS: Significantly elevated SCEL expression in PTC tissues versus normal controls (P < 0.01). Higher SCEL levels in recurrent PTC versus non-recurrent PTC (P < 0.01), correlating with increased recurrence risk. SCEL expression levels were significantly correlated with TNM stage, AJCC stage, and I-131 treatment status (P < 0.01). Lower SCEL expression predicted significantly improved prognosis in recurrent PTC patients. Multivariate Cox analysis confirmed low SCEL as an independent protective factor for disease-free survival (DFS) (HR = 0.358, 95 % CI: 0.149-0.861, P = 0.022). Recurrence showed no significant association with EMT pathways. This prognostic advantage was mechanistically linked to enhanced tumor immune cell infiltration in the low-SCEL group (P < 0.01), whereas high SCEL correlated with an immunosuppressive microenvironment.
CONCLUSIONS: This study identifies SCEL as a recurrence-associated potential biomarker in PTC. Critically, lower SCEL expression may serve as a potential independent protective factor, predicting improved DFS in recurrent PTC patients. This survival benefit is mediated through modulation of the tumor immune microenvironment rather than EMT pathways.