Article Text


Original research
S100A4 amplifies TGF-β-induced epithelial–mesenchymal transition in a pleural mesothelial cell line
  1. Qian Ning,
  2. Feiyan Li,
  3. Lei Wang,
  4. Hong Li,
  5. Yan Yao,
  6. Tinghua Hu,
  7. Zhongmin Sun
  1. Department of Respiration and Critical Care Medicine, The First Hospital Affiliated to School of Medicine of Xi’an Jiaotong University, Shaanxi, China
  1. Correspondence to Dr Zhongmin Sun, Department of Respiration andCritical care medicine, The First hospital Affiliatedto School of Medicine of Xi’an Jiaotong University, Xi’an, Shaanxi, China; ningqian2012{at}


Pleural fibrosis can dramatically lower the quality of life. Numerous studies have reported that epithelial–mesenchymal transition (EMT) regulated by transforming growth factor-β (TGF-β) is involved in fibrosis. However, the molecular mechanism is inadequately understood. Fibroblast-specific protein-1 (S100A4) is a target of TGF-β signaling. In our previous study, we have reported that S100A4 is highly expressed in pleural fibrosis. Thus, we suggest that S100A4 took part in the TGF-β-induced EMT in pleural fibrosis. In this study, we determined the expression of S100A4 and EMT-related markers in Met-5A cells (pleural mesothelial cells) treated with TGF-β or TGF-β inhibitor by real-time PCR and western blot. In order to explore the role of S100A4, we used siRNA to knock down the expression of S100A4 in cell model. We found that the expression of epithelial cell marker was decreased and the mesenchymal cell marker increased with S100A4 upregulation after treatment with TGF-β. Moreover, the changes of EMT-related event were restricted when the expression of S100A4 was knocked down. Conversely, S100A4 can partially rescue the EMT-related expression changes induced by TGF-β inhibitor. These findings suggest that S100A4 expression is induced by the TGF-β pathway, and silencing S100A4 expression can inhibit the process of TGF-β-induced EMT.

  • transforming growth factors
  • fibroblast growth factors
  • Phenotype
  • chronic disease

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  • Contributors QN, FL, LW, HL, YY and TH carried out the experiments, ZS designed the study, and QN and ZS prepared the manuscript. All authors read and approved the final manuscript.

  • Funding This study was supported by the National Natural Science Foundation of China (81170073).

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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