Osterix promotes the migration and angiogenesis of breast cancer by upregulation of S100A4 expression.

As a key transcription factor required for bone formation, osterix (OSX) has been reported to be overexpressed in various cancers, however, its roles in breast cancer progression remain poorly understood. In this study, we demonstrated that OSX was highly expressed in metastatic breast cancer cells. Moreover, it could upregulate the expression of S100 calcium binding protein A4 (S100A4) and potentiate breast cancer cell migration and tumor angiogenesis in vitro and in vivo. Importantly, inhibition of S100A4 impaired OSX-induced cell migration and capillary-like tube formation. Restored S100A4 expression rescued OSX-short hairpin RNA-suppressed cell migration and capillary-like tube formation. Moreover, the expression levels of OSX and S100A4 correlated significantly in human breast tumors. Our study suggested that OSX acts as an oncogenic driver in cell migration and tumor angiogenesis, and may serve as a potential therapeutic target for human breast cancer treatment. © 2018 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.

Citation

Shuang Qu, Jiahui Wu, Qianyi Bao, Bing Yao, Rui Duan, Xiang Chen, Lingyun Li, Hongyan Yuan, Yucui Jin, Changyan Ma. Osterix promotes the migration and angiogenesis of breast cancer by upregulation of S100A4 expression. Journal of cellular and molecular medicine. 2019 Feb;23(2):1116-1127

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PMID: 30450809

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