ArticleFrontiers in oncology2025
CD9 regulates proliferation, invasion, migration and radioresistance of esophageal squamous cell carcinoma by activating AKT/GSK3β signaling pathway.
Article in Frontiers in oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed.
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Radioresistance poses a major therapeutic challenge in ESCC, significantly impacting patient prognosis. CD9, as a crucial membrane regulatory protein, exhibits dual regulatory roles in various cancers, yet its precise mechanism in ESCC radioresistance remains unclear. This study aims to systematically elucidate the molecular mechanisms by which CD9 regulates malignant phenotypes and radiosensitivity through the AKT/GSK3β signaling pathway in ESCC. Methods: TCGA data, ESCC tissues microarray, Results: TCGA data analysis and 32 paired ESCC and adjacent non-tumorous tissues microarray revealed that CD9 expression was higher in ESCC tissues than in normal tissues, and was associated with tumor stage or lymph node metastasis. Functional validation demonstrated CD9 overexpression in Eca109 cells augmented proliferation, migration and invasion capacity, while enhancing radioresistance (SF2 increased from 0.488 to 0.596, SER decreasing to 0.888). Conversely, CD9 knockdown in TE13 cells reduced SF2 from 0.579 to 0.461, and SER up to 1.244. Mechanistically, CD9 modulated p-AKT (ser473) and p-Gsk3β (ser9) levels increased to 1.95-fold and 1.42-fold in overexpression models, respectively, with 58% and 33% reductions in knockdown group. TCGA cohort analysis (n=82) revealed no significant OS/DSS/PFI differences by CD9 expression Conclusions: CD9 promotes ESCC progression and radioresistance by activating the AKT/GSK3β pathway and holds promise as a potential prognostic biomarker and therapeutic target for ESCC.
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