Department of Pathology, The First Affiliated Hospital of Zhengzhou University, and Department of Microbiology and Immunology, College of Basic Medicine, Zhengzhou University, 40 Daxue Road, Zhengzhou, Henan Province, 450052, People's Republic of China.
Mol Biol Rep. 2012 Jan;39(1):199-208. doi: 10.1007/s11033-011-0726-1. Epub 2011 May 21.
It is well documented that S100A4 is upregulated in a large amount of invasive tumors and plays a pivotal role in tumor invasion and metastasis. However, the precise role and mechanism S100A4 exerts in the invasion and metastasis of esophageal squamous cell carcinoma (ESCC) have not been fully elucidated to date. Our data demonstrated that S100A4 was overexpressed in human ESCC tissues, especially in ESCC with poor differentiation, deep invasion and lymph node metastasis. Subsequently, the knockdown of S100A4 by RNAi in ESCC cell line (EC-1) could reduce cell invasion, metastasis and proliferation ability in vitro. Most importantly, S100A4 regulated MMP-2 positively and E-cadherin negatively in vivo and in vitro to some extent. Our results suggest that S100A4 is an important factor in the invasion, metastasis and proliferation of ESCC and may control invasion and metastasis at least in part through the regulation of MMP-2 and E-cadherin activity. S100A4 may serve as a biomarker for progression of ESCC and a potential molecular target for biotherapy of ESCC.
有大量文献记载 S100A4 在大量侵袭性肿瘤中上调，并且在肿瘤侵袭和转移中发挥关键作用。然而，S100A4 在食管鳞状细胞癌（ESCC）侵袭和转移中的确切作用和机制尚未完全阐明。我们的数据表明，S100A4 在人 ESCC 组织中过表达，尤其是在分化不良、浸润深和淋巴结转移的 ESCC 中。随后，在 ESCC 细胞系（EC-1）中通过 RNAi 敲低 S100A4 可降低体外细胞侵袭、转移和增殖能力。最重要的是，S100A4 可在体内和体外在一定程度上正向调节 MMP-2，负向调节 E-钙粘蛋白。我们的结果表明，S100A4 是 ESCC 侵袭、转移和增殖的重要因素，至少部分通过调节 MMP-2 和 E-钙粘蛋白活性来控制侵袭和转移。S100A4 可作为 ESCC 进展的生物标志物，也是 ESCC 生物治疗的潜在分子靶点。
