S100A4 mediated cell invasion and metastasis of esophageal squamous cell carcinoma via the regulation of MMP-2 and E-cadherin activity

• Published in: Molecular biology reports Vol. 39; no. 1; pp. 199 - 208
• Main Authors: Zhang, Hong-Yan, Zheng, Xian-Zhao, Wang, Xin-Hua, Xuan, Xiao-Yan, Wang, Feng, Li, Shan-Shan
• Format: Journal Article
• Language: English
• Published: Dordrecht Springer Netherlands 01.01.2012; Springer Nature B.V
• Subjects: Animal Anatomy; Animal Biochemistry; Biomarkers; Biomedical and Life Sciences; Blotting, Western; Cadherins - metabolism; Cancer; Carcinoma, Squamous Cell - metabolism; Carcinoma, Squamous Cell - physiopathology; Cellular biology; DNA Primers - genetics; Esophageal Neoplasms - metabolism; Esophageal Neoplasms - physiopathology; Esophagus; Gene expression; Gene Expression Regulation, Neoplastic - genetics; Gene Expression Regulation, Neoplastic - physiology; Histology; Humans; Immunohistochemistry; Life Sciences; Matrix Metalloproteinase 2 - metabolism; Metastasis; Molecular biology; Morphology; Neoplasm Invasiveness - physiopathology; Neoplasm Metastasis - physiopathology; Real-Time Polymerase Chain Reaction; S100 Calcium-Binding Protein A4; S100 Proteins - metabolism; Tetrazolium Salts; Thiazoles; Esophageal squamous cell carcinoma; S100A4; Metastasis; Invasion
• ISSN: 0301-4851; 1573-4978
• DOI: 10.1007/s11033-011-0726-1

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.