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Up-regulation of SPOCK1 induces epithelial–mesenchymal transition and promotes migration and invasion in esophageal squamous cell carcinoma
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  • 作者:Xiaopeng Song ; Ping Han ; Jingmei Liu ; Yunwu Wang…
  • 关键词:SPOCK1 ; Epithelial–mesenchymal transition ; Esophageal squamous cell carcinoma ; Migration ; Invasion
  • 刊名:Journal of Molecular Histology
  • 出版年:2015
  • 出版时间:October 2015
  • 年:2015
  • 卷:46
  • 期:4-5
  • 页码:347-356
  • 全文大小:6,165 KB
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  • 作者单位:Xiaopeng Song (1) (2)
    Ping Han (1)
    Jingmei Liu (1)
    Yunwu Wang (1)
    Dongxiao Li (1)
    Jiayi He (1)
    Jin Gong (1)
    Mengke Li (1)
    Wei Tu (1)
    Wei Yan (1)
    Mei Liu (1)
    Huanjun Huang (1)
    Dean Tian (1)
    Jiazhi Liao (1)

    1. Department of Gastroenterology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095# Jiefang Avenue, Wuhan, 430030, Hubei Province, China
    2. Department of Gastroenterology, The Second Affiliated Hospital of Zhengzhou University, 2 Jingba Road, Zhengzhou, 450014, Henan Province, China
  • 刊物类别:Biomedical and Life Sciences
  • 刊物主题:Life Sciences
    Cell Biology
    Biomedicine
    Developmental Biology
  • 出版者:Springer Netherlands
  • ISSN:1567-2387
文摘
Invasion and metastasis are the major causes of death in patients with esophageal squamous cell carcinoma (ESCC). Recent studies have confirmed that SPARC/osteonectin, cwcv and kazal-like domains proteoglycan 1 (SPOCK1) plays multiple roles in cancer progression. This study aims to explore the clinical characteristics of SPOCK1 in ESCC and its roles in the migration and invasion of ESCC cell lines. In this study, the up-regulation of SPOCK1 expression was frequently detected in primary ESCC tumor tissues compared with those in non-tumor tissues, which was significantly associated with tumor invasion (p?=?0.004) and distant metastasis (p?=?0.010). SPOCK1 was expressed at higher level in TE13 cells as compared to the low malignant Eca109 and TE1 cells. Overexpression of SPOCK1 in Eca109 cells decreased the expressions of epithelial marker E-cadherin and ZO-1, while increased mesenchymal marker Vimentin and N-cadherin levels. After ectopic expression of SPOCK1, Eca109 cells exhibited a morphological change from an epithelial cobblestone phenotype to an elongated fibroblastic phenotype, concomitant with cytoskeletal rearrangements and increased migration and invasion, suggesting that EMT occurs. While silencing SPOCK1 in TE13 cells had the opposite effects. These results suggest that up-regulation of SPOCK1 in ESCC induces EMT, thus promotes migration and invasion in ESCC cells.

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