Osterix promotes the migration and angiogenesis of breast cancer by upregulation of S100A4 expression
Osterix promotes the migration and angiogenesis of breast cancer by upregulation of S100A4 expression
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Osterix 通过上调 S100A4 表达促进乳腺癌的迁移和血管生成。
DOI：
10.1111/jcmm.14012
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发表时间：
2019-02-01
影响因子：
5.3
通讯作者：
Ma, Changyan
中科院分区：
文献类型：
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作者：
Qu, Shuang;Wu, Jiahui;Ma, Changyan
作为骨形成所需的关键转录因子，osterix (OSX) 据报道在多种癌症中过度表达，然而，其在乳腺癌进展中的作用仍知之甚少。在这项研究中，我们证明 OSX 在转移性乳腺癌细胞中高表达。此外，它还可以上调 S100 钙结合蛋白 A4 (S100A4) 的表达，并在体外和体内增强乳腺癌细胞迁移和肿瘤血管生成。重要的是，抑制 S100A4 会损害 OSX 诱导的细胞迁移和毛细管样管形成。恢复的 S100A4 表达挽救了 OSX 短发夹 RNA 抑制的细胞迁移和毛细管样管形成。此外，OSX和S100A4的表达水平在人类乳腺肿瘤中显着相关。我们的研究表明，OSX 在细胞迁移和肿瘤血管生成中充当致癌驱动因素，并可能作为人类乳腺癌治疗的潜在治疗靶点。
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.