Radiology and oncology · 2026
EPHA3, upregulated in high-risk histological subtypes of gastrointestinal stromal tumor, promotes GIST progression.
СтатьяНазвание и аннотация: Перевод в очереди
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Wei Han, Zhao Jia, Wang Hongmei, Guo Lihong, Liu Yanhong, Wang Chuntao, Yang Liang, Qi Zhi, Tian Wencong, Cao Lei, Gao Yang
Аннотация
BACKGROUND: To explore the expression pattern and functional role of EPH receptor A3 (EPHA3) in high-risk gastrointestinal stromal tumors (GISTs) and its potential relevance to tumor progression.
MATERIALS AND METHODS: Immunohistochemical (IHC) analysis was performed to evaluate EPHA3 expression across a pilot cohort of clinical GIST specimens with different risk stratifications. The biological functions of EPHA3 in vitro were assessed using (5-ethynyl-2'-deoxyuridine, EdU) assay, colony formation, apoptosis, wound-healing, and transwell assays in EPHA3-knockout GIST-430 cells. Furthermore, RNA sequencing (RNA-seq) analysis was utilized to identify differentially expressed genes and associated signaling pathways following EPHA3 knockout.
RESULTS: EPHA3 expression was found to be elevated in high-risk GIST specimens compared with intermediate-risk cases. Loss-of-function assays demonstrated that EPHA3 knockout attenuated cell proliferation and migration while promoting apoptosis in vitro. Pathway enrichment analysis suggested that EPHA3 expression is associated with cell adhesion, extracellular matrix interaction, and mesenchymal-related phenotypic remodeling.
CONCLUSIONS: Our findings suggest that EPHA3 is upregulated in high-risk GIST and contributes to aggressive cellular behavior in vitro. These preliminary data indicate that EPHA3 may play a role in the malignant progression of GIST, although its clinical utility as a biomarker requires further validation in larger cohorts.
MATERIALS AND METHODS: Immunohistochemical (IHC) analysis was performed to evaluate EPHA3 expression across a pilot cohort of clinical GIST specimens with different risk stratifications. The biological functions of EPHA3 in vitro were assessed using (5-ethynyl-2'-deoxyuridine, EdU) assay, colony formation, apoptosis, wound-healing, and transwell assays in EPHA3-knockout GIST-430 cells. Furthermore, RNA sequencing (RNA-seq) analysis was utilized to identify differentially expressed genes and associated signaling pathways following EPHA3 knockout.
RESULTS: EPHA3 expression was found to be elevated in high-risk GIST specimens compared with intermediate-risk cases. Loss-of-function assays demonstrated that EPHA3 knockout attenuated cell proliferation and migration while promoting apoptosis in vitro. Pathway enrichment analysis suggested that EPHA3 expression is associated with cell adhesion, extracellular matrix interaction, and mesenchymal-related phenotypic remodeling.
CONCLUSIONS: Our findings suggest that EPHA3 is upregulated in high-risk GIST and contributes to aggressive cellular behavior in vitro. These preliminary data indicate that EPHA3 may play a role in the malignant progression of GIST, although its clinical utility as a biomarker requires further validation in larger cohorts.