SDCBP Cooperates With YBX1 to Promote ESCC Metastasis by Forming a Positive Feedback Loop With Wnt‐β‐Catenin Signaling Pathway
Syndecan binding protein (SDCBP) has been shown to be upregulated in esophageal squamous cell carcinoma (ESCC) and predicts poor prognosis in our previous research. SDCBP stimulated the proliferation and tumor formation and may be a target for ESCC. However, the participation of SDCBP in epithelial-mesenchymal transition (EMT) and ESCC metastasis is unclear. In this study, we found that SDCBP promoted the EMT process of ESCC cells and facilitated ESCC metastasis both in vitro and in vivo. Mechanically, SDCBP was found to influence the activation of the Wnt-β-catenin pathway. β-catenin expression and nuclear localization were regulated by SDCBP, accompanied by altered expression of Wnt-β-catenin pathway target genes. Additionally, SDCBP interacted with Y-box binding protein 1 (YBX1) and abnormally upregulated YBX1 in ESCC was responsible for SDCBP-mediated regulation of ESCC migration and invasion. Finally, SDCBP was identified to be transcriptionally regulated by the Wnt-β-catenin pathway. Thus, our study provides a better understanding of the SDCBP-YBX1-Wnt-β-catenin axis in ESCC metastasis and explores a positive feedback loop between SDCBP and the Wnt-β-catenin pathway, offering more compelling evidence for employing SDCBP as a target for ESCC treatment.
Authors
- Bo Bian (ORCID: https://orcid.org/0000-0002-0264-5473)
- Guangji Zhang (ORCID: https://orcid.org/0000-0003-4525-9422)
- Kai Li (ORCID: https://orcid.org/0000-0002-0318-7064)
- Li Han (ORCID: https://orcid.org/0000-0002-4486-0534)
- Chen Yuan (ORCID: https://orcid.org/0000-0003-4239-352X)
- Ruijuan Du
- Kelei Guo
- Hui Zhang
- Manyu Luo
Institutions
- Zhejiang Chinese Medical University (CN)
- Nanyang Institute of Technology (CN)
Publication Details
- Journal
- Journal of Biochemical and Molecular Toxicology
- Published
- 2026-07-28
- DOI
- https://doi.org/10.1002/jbt.71046
- Primary Topic
- Proteoglycans and glycosaminoglycans research
- Type
- article
- Field-Weighted Citation Impact
- 0.00