Open AccessOverexpression of metadherin mediates metastasis of osteosarcoma by regulating epithelial–mesenchymal transition
Author(s) -
Tang J.,
Shen L.,
Yang Q.,
Zhang C.
Publication year - 2014
Publication title -
cell proliferation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.647
H-Index - 74
eISSN - 1365-2184
pISSN - 0960-7722
DOI - 10.1111/cpr.12129
Subject(s) - osteosarcoma , epithelial–mesenchymal transition , mesenchymal stem cell , metastasis , cancer research , microbiology and biotechnology , chemistry , biology , cancer , genetics
Objectives Osteosarcoma ( OS ) is one of the most common primary malignant bone tumours of childhood and adolescence, and is characterized by high propensity for metastasis (specially to the lung), which is the main cause of death. However, molecular mechanisms underlying metastasis of OS are still poorly understood. Materials and methods Metadherin ( MTDH ) was identified to be significantly upregulated in OS tissues that had metastasized compared to OS without metastasis, using a two‐dimensional approach of electrophoresis, coupled with mass spectrometry. To understand the function of MTDH in OS , OS cell lines U2 OS and SOSP ‐M were transfected with retroviral sh RNA vector against MTDH . Results It was found that metastatic propensity as well as cell proliferation were significantly reduced in both U2 OS and SOSP ‐M. Migration and invasion of U2 OS and SOSP ‐M cells were significantly lower after knock‐down of MTDH . In addition, epithelial–mesenchymal transition ( EMT ) was reduced after knock‐down of MTDH . Clinicopathologically, overexpression of MTDH was significantly associated with metastasis and poor survival of patients with OS . Conclusion Taken together, our results demonstrate that MTDH mediated metastasis of OS through regulating EMT . This could be an ideal therapeutic target against metastasis of OS .