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CD24 mediates gastric carcinogenesis and promotes gastric cancer progression via STAT3 activation
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  • 作者:Ying-Chao Wang (1)
    Ji-Lin Wang (1)
    Xuan Kong (1)
    Tian-Tian Sun (1)
    Hao-Yan Chen (1)
    Jie Hong (1)
    Jing-Yuan Fang (1)
  • 关键词:CD24 ; Early event ; Gastric carcinogenesis ; STAT3
  • 刊名:Apoptosis
  • 出版年:2014
  • 出版时间:April 2014
  • 年:2014
  • 卷:19
  • 期:4
  • 页码:643-656
  • 全文大小:10,834 KB
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  • 作者单位:Ying-Chao Wang (1)
    Ji-Lin Wang (1)
    Xuan Kong (1)
    Tian-Tian Sun (1)
    Hao-Yan Chen (1)
    Jie Hong (1)
    Jing-Yuan Fang (1)

    1. GI Division, Ren Ji Hospital, School of Medicine, Shanghai Jiao-Tong University, Shanghai Institution of Digestive Disease, Key Laboratory of Gastroenterology & Hepatology, Ministry of Health (Shanghai Jiao-Tong University), State Key Laboratory of Oncogene and Related Genes, 145 Middle Shandong Rd., Shanghai, 200001, China
  • ISSN:1573-675X
文摘
The development of gastric cancer (GC) is a complex multistep process, including numerous genetic and epigenetic changes. CD24 is associated with enhanced invasiveness of GC and a poor prognosis. However, the mechanism by which CD24 induces GC progression remains poorly characterized. Here, we found that the expression of CD24 gradually increased in samples of normal gastric mucosa, non-atrophic chronic gastritis, chronic atrophic gastritis (CAG), CAG with intestinal metaplasia, dysplasia and GC. Moreover, the knockdown of CD24 induced significant levels of apoptosis in GC cells via the mitochondrial apoptotic pathway. CD24 may also promote cellular invasion and regulate the expression of E-cadherin, fibronectin and vitamin D receptor in GC cells. The activation of signal transducer and activator of transcription 3 (STAT3) may mediate CD24-induced GC survival and invasion in vitro. Furthermore, CD24-induced GC progression and STAT3 activation could also be detected in vivo and in clinical GC tissues samples. Taken together, our results indicate that CD24 mediates gastric carcinogenesis and may promote GC progression by suppressing apoptosis and promoting invasion, with the activation of STAT3 playing a critical role.

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