Objective:

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, which is crucial for tumor progression in TNBC.

Key Findings:

• SOX10 overexpression promoted proliferation, migration, and invasion in TNBC cells (P<0.05).
• SOX10 knockdown inhibited these abilities (P<0.05).
• SOX10 upregulated mesenchymal markers and Wnt/β-catenin pathway components while downregulating E-cadherin (P<0.05).
• Wnt pathway activation reversed EMT suppression from SOX10 knockdown (P<0.05).
• Wnt pathway inhibition attenuated EMT promotion from SOX10 overexpression (P<0.05).

Interpretation:

SOX10 enhances malignant behaviors in TNBC cells via the Wnt/β-catenin signaling pathway and EMT induction, suggesting it may serve as a promising therapeutic target.

Limitations:

• Study primarily focused on in vitro experiments; in vivo validation needed.
• Mechanistic details of SOX10's role in other signaling pathways remain unexplored.
• The clinical relevance of findings and the need for patient-derived models should be addressed.

Conclusion:

The SOX10-Wnt/β-catenin axis may serve as a promising therapeutic target for TNBC, necessitating further investigation.