Open AccessOsterix promotes the migration and angiogenesis of breast cancer by upregulation of S100A4 expression
Author(s) -
Qu Shuang,
Wu Jiahui,
Bao Qianyi,
Yao Bing,
Duan Rui,
Chen Xiang,
Li Lingyun,
Yuan Hongyan,
Jin Yucui,
Ma Changyan
Publication year - 2019
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.14012
Subject(s) - angiogenesis , downregulation and upregulation , cancer research , cell migration , breast cancer , transcription factor , small hairpin rna , cell growth , chemistry , cell , biology , microbiology and biotechnology , cancer , medicine , cell culture , gene knockdown , gene , biochemistry , genetics
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.