Metastasin leads to poor prognosis of hepatocellular carcinoma through partly inducing EMT

Zheng,Xin; Gai,Xiaohong; Wu,Zhenhua; Liu,Qingguang; Yao,Yingmin

doi:10.3892/or.2013.2341

Metastasin leads to poor prognosis of hepatocellular carcinoma through partly inducing EMT

Authors:
- Xin Zheng
- Xiaohong Gai
- Zhenhua Wu
- Qingguang Liu
- Yingmin Yao
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Affiliations: Department of Hepatobiliary Surgery, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, P.R. China, Department of Thoracic Surgery, Xinjiang Tumor Hospital, Urumqi, Xinjiang 830002, P.R. China
Published online on: March 12, 2013 https://doi.org/10.3892/or.2013.2341
Pages: 1811-1818

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Abstract

Hepatocellular carcinoma (HCC) is a common malignant cancer worldwide characterized by high metastatic potential and poor prognosis following radical resection. Metastasin is a Ca2+-binding protein associated with tumor metastasis. However, the expression and function of metastasin remain unknown. In the present study, we found that the expression of metastasin was upregulated in HCC tissues and positively correlated with poor prognosis following radical resection. Ectopic expression of metastasin in vitro induced typical epithelial-mesenchymal transition (EMT) in Hep3B cells including higher capacity of both migration and invasion, increased expression of both Vimentin and N-cadherin and decreased expression of E-cadherin. Knockdown of metastasin produced the opposite results in MHCC97H cells, which indicates that metastasin promotes HCC progression via induction of EMT. SNAI1 expression was upregulated by enforced expression of metastasin and, consequently, suppressing upregulation of SNAI1 secondary to metastasin overexpression abolished EMT. Collectively, the present results suggest that metastasin leads to HCC EMT partly through upregulating SNAI1 and contributes to poor prognosis following radical liver resection.

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