ArticleMolecular carcinogenesis2026
EphA2/SHP2/SOX8 Axis: A Novel Target for Regulation of Migration and Cetuximab Treatment Sensitivity in Oral Squamous Cell Carcinoma.
Article in Molecular carcinogenesis, 2026. 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.
The trial behind it
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Who cites it
1 citing paper in PubMed.
- EphA2/SHP2/SOX8 Axis: A Novel Target for Regulation of Migration and Cetuximab Treatment Sensitivity in Oral Squamous Cell Carcinoma.Molecular carcinogenesis · 2026Article
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Authors and funding
4 authors.
Funding
Abstract
The development of resistance to anticancer therapies in cancer cell is a major challenge in the treatment of oral squamous cell carcinoma (OSCC), a common malignant tumor. Erythropoietin-producing hepatocellular A2 (EphA2) affects several cancers, and this study examined its role in enhancing OSCC. Following screening, EphA2 and SRY-Box transcription factor 8 (SOX8) knocked down and overexpression cell lines were constructed, followed by treatment with Cetuximab. Quantitative real-time polymerase chain reaction, western blot, cell counting kit-8, wound healing, and transwell assay were used to detect the relevant indicators. Co-immunoprecipitation was used to detect the interaction between EphA2 and SH2 domain-containing protein-tyrosine phosphatase-2 (SHP2). Double luciferase reporter gene experiment and chromatin immunoprecipitation experiment were performed to verify the regulatory mechanism of EphA2 and SOX8. The mouse tumor model was established, and the tumor development was observed after plasmid transfection and Cetuximab treatment. EphA2 was highly expressed in OSCC cells, and overexpression of EphA2 up-regulated SOX8. EphA2 regulated SOX8 and associated protein expression to increase OSCC cell migration and invasion. EphA2 knockdown made OSCC cells more sensitive to Cetuximab, whereas SOX8 overexpression reduced this sensitivity. We found SHP2 bound to SOX8. Down-regulation of EphA2 decreased tumor growth in mice, increased Cetuximab sensitivity, and overexpression of SOX8/SHP2 decreased Cetuximab sensitivity. OSCC had elevated EphA2 levels, which enhanced cell migration and invasion via SHP2/SOX8 and impaired Cetuximab sensitivity. Down-regulation of EphA2 decreased tumor growth and enhanced Cetuximab sensitivity, suggesting new OSCC targets and potential treatments.
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