ArticleFrontiers in oncology2026
Effects of SOX10 on the proliferative, invasive, migratory, and epithelial-mesenchymal transition abilities of triple-negative breast cancer cells.
Article in Frontiers in oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Triple-negative breast cancer (TNBC) is a highly aggressive subtype of breast cancer with limited targeted therapeutic options. Sry-related HMG-box gene 10 (SOX10) has been implicated in tumor progression in various malignancies, but its functional role and underlying mechanism in TNBC remain unclear. This study aimed to investigate the effect of SOX10 on TNBC cell proliferation, metastasis, and epithelial-mesenchymal transition (EMT), and to explore its association with the Wnt/β-catenin signaling pathway. Methods: HCC1937 cells (high endogenous SOX10 expression) and MDA-MB-453 cells (low endogenous SOX10 expression) were used for SOX10 knockdown and overexpression experiments. Wnt pathway activators and inhibitors were applied in rescue experiments to validate the mechanistic link. Cell proliferation was assessed by CCK-8 assay; migration and invasion were evaluated by scratch wound and Transwell assays, respectively. The expression levels of EMT markers and Wnt/β-catenin pathway-related proteins were quantified by Western blot analysis. Results: SOX10 overexpression significantly promoted proliferation, migration, and invasion in both TNBC cell lines, while SOX10 knockdown markedly inhibited these abilities (all P<0.05). SOX10 upregulated the expression of mesenchymal markers (Vimentin, N-cadherin) and Wnt/β-catenin pathway components (WNT1, nuclear β-catenin, C-myc, Cyclin D1), and downregulated the epithelial marker E-cadherin (all P<0.05). Rescue experiments confirmed that Wnt pathway activation reversed the EMT suppression induced by SOX10 knockdown, while Wnt pathway inhibition attenuated the EMT promotion caused by SOX10 overexpression (all P<0.05). Discussion: SOX10 promotes malignant biological behaviors in TNBC cells by activating the Wnt/β-catenin signaling pathway and inducing EMT. These findings suggest that the SOX10-Wnt/β-catenin axis may serve as a potential therapeutic target for TNBC, warranting further mechanistic and translational investigation.
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