Wnt5a promotes migration of human osteosarcoma cells by triggering a phosphatidylinositol-3 kinase/Akt signals
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  • 作者:Ailiang Zhang (1)
    Shuanghua He (1)
    Xiaoliang Sun (1)
    Lianghua Ding (1)
    Xinnan Bao (1)
    Neng Wang (1)
  • 关键词:Wnt5a ; PI3K ; Akt ; Osteosarcoma ; Migration
  • 刊名:Cancer Cell International
  • 出版年:2014
  • 出版时间:December 2014
  • 年:2014
  • 卷:14
  • 期:1
  • 全文大小:828 KB
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  • 作者单位:Ailiang Zhang (1)
    Shuanghua He (1)
    Xiaoliang Sun (1)
    Lianghua Ding (1)
    Xinnan Bao (1)
    Neng Wang (1)

    1. Department of Orthopaedics, Changzhou No. 1 People’s Hospital, Changzhou, Jiangsu, 213003, PR China
  • ISSN:1475-2867
文摘
Wnt5a is classified as a non-transforming Wnt family member and plays complicated roles in oncogenesis and cancer metastasis. However, Wnt5a signaling in osteosarcoma progression remains poorly defined. In this study, we found that Wnt5a stimulated the migration of human osteosarcoma cells (MG-63), with the maximal effect at 100?ng/ml, via enhancing phosphorylation of phosphatidylinositol-3 kinase (PI3K)/Akt. PI3K and Akt showed visible signs of basal phosphorylation and elevated phosphorylation at 15?min after stimulation with Wnt5a. Pharmaceutical inhibition of PI3K with LY294002 significantly blocked the Wnt5a-induced activation of Akt (p-Ser473) and decreased Wnt5a-induced cell migration. Akt siRNA remarkably inhibited Wnt5a-induced cell migration. Additionally, Wnt5a does not alter the total expression and phosphorylation of β-catenin in MG-63 cells. Taken together, we demonstrated for the first time that Wnt5a promoted osteosarcoma cell migration via the PI3K/Akt signaling pathway. These findings could provide a rationale for designing new therapy targeting osteosarcoma metastasis.

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