S100A6 expression and function in human osteosarcoma
S100A6 expression and function in human osteosarcoma
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DOI：
10.1007/s11999-008-0361-x
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发表时间：
2008-09-01
影响因子：
4.2
通讯作者：
Luu, Hue H.
中科院分区：
文献类型：
--
作者：
Luo, Xiaoji;Sharff, Katie A.;Luu, Hue H.
有一个关键的需要，以确定标记，可以准确地识别现有的或预测未来的转移性疾病的骨肉瘤患者，因为大多数患者目前与不可检测的微转移性疾病。我们以前报道过S100A6在人骨肉瘤中过表达，免疫组化显示S100A6表达增加与临床转移减少相关。我们从骨肉瘤患者的活检组织中建立了11个原代培养物，11个原代培养物中有10个相对于正常人成骨细胞S100A6的表达增加。为了进一步探讨以前报道的转移抑制的可能机制，我们在本报告中使用siRNA介导的S100A6基因敲减在四个常用的人骨肉瘤细胞系中，然后检查它们的细胞粘附，迁移和侵袭特性。敲低S100A6表达可抑制细胞粘附，促进细胞迁移和侵袭。相反，S100A6过表达增强细胞粘附并抑制细胞侵袭。我们的数据表明，S100A6通常在人骨肉瘤中过表达。S100A6可能通过促进细胞粘附、抑制细胞运动和侵袭而抑制骨肉瘤转移。因此，S100A6可能被认为是人类骨肉瘤的潜在标志物，具有识别无转移患者的预后价值。
There is a critical need to identify markers that can accurately identify existing or predict future metastatic disease in patients with osteosarcoma since the majority of patients present with undetectable micrometastatic disease. We previously reported S100A6 is overexpressed in human osteosarcoma and increased expression of S100A6 by immunohistochemistry correlated with decreased clinical metastasis. We have established 11 primary cultures from biopsies of patients with osteosarcoma and ten of the 11 primary cultures have increased expression of S100A6 relative to normal human osteoblasts. To further explore possible mechanisms for metastasis suppression previously reported, we used in this report siRNA-mediated knockdown of S100A6 in four commonly used human osteosarcoma lines, then examined their cell adhesion, migration, and invasion properties. Knockdown of S100A6 expression inhibited cell adhesion and promoted cell migration and invasion in these lines. Conversely, S100A6 overexpression enhanced cell adhesion and inhibited cell invasion. Our data demonstrate S100A6 is commonly overexpressed in human osteosarcoma. S100A6 may inhibit osteosarcoma metastasis by promoting cell adhesion and inhibiting cell motility and invasion. Thus, S100A6 may be considered a potential marker for human osteosarcoma with prognostic value for identifying patients without metastases.