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上皮间质转化在血管生成拟态中的研究进展

孔祥琳综述, 程先硕, 杨之斌, 李云峰审校

孔祥琳综述, 程先硕, 杨之斌, 李云峰审校. 上皮间质转化在血管生成拟态中的研究进展[J]. 肿瘤防治研究, 2014, 41(04): 405-408. DOI: 10.3971/j.issn.1000-8578.2014.04.027
引用本文: 孔祥琳综述, 程先硕, 杨之斌, 李云峰审校. 上皮间质转化在血管生成拟态中的研究进展[J]. 肿瘤防治研究, 2014, 41(04): 405-408. DOI: 10.3971/j.issn.1000-8578.2014.04.027
KONG Xianglin, CHENG Xianshuo, YANG Zhibin, LI Yunfeng. Contribution of Epithelial-mesenchymal Transition to Vasculogenic Mimicry[J]. Cancer Research on Prevention and Treatment, 2014, 41(04): 405-408. DOI: 10.3971/j.issn.1000-8578.2014.04.027
Citation: KONG Xianglin, CHENG Xianshuo, YANG Zhibin, LI Yunfeng. Contribution of Epithelial-mesenchymal Transition to Vasculogenic Mimicry[J]. Cancer Research on Prevention and Treatment, 2014, 41(04): 405-408. DOI: 10.3971/j.issn.1000-8578.2014.04.027

上皮间质转化在血管生成拟态中的研究进展

基金项目: 国家自然科学基金资助项目 (30960455);云南省科技厅计划基金资助项目 (2008ZC142M)
详细信息
    作者简介:

    孔祥琳综述: 孔祥琳(1986-),女,硕士在读,主要从事结直肠癌抗血管生成基础及临床研究

    通讯作者:

    李云峰审校: 李云峰,E-mail:liyunfeng@medmail.com.cn

  • 中图分类号: R73-37

Contribution of Epithelial-mesenchymal Transition to Vasculogenic Mimicry

  • 摘要: 肿瘤的侵袭转移受到多种因素调节,其中血管生成拟态(vasculogenic mimicry,VM)作为已被发现的一种微循环的新模式,是患者预后不良的一个关键因素。近年研究表明上皮间质转化(epithelial-mesenchymal transition,EMT)在VM形成中发挥重要作用。本文就最新研究,综述EMT 相关核转录因子,EMT细胞表达的干细胞特性,EMT细胞导致肿瘤微环境成分的改变在VM形成中的作用,并简要探讨VM、EMT、肿瘤干细胞(cancer stem cells??CSCs)以及微环境之间的关系。鉴于EMT在VM的形成中的重要作用,深入开发抗VM形成的药物以及研究EMT形成机制有望为靶向EMT 抑制VM形成治疗肿瘤远处转移的新策略提供扎实的理论基础。

     

    Abstract: As a new model of the microcirculation, tumor cell vasculogenic mimicry (VM) is an unfavorable prognostic factor for tumor patients. Recent studies have showed that epithelial-mesenchymal transition (EMT) plays an important role in VM formation. In this review, we present evidences for the participation of nuclear factors which regulate EMT, stem cell characteristics of EMT cells and microenvironment changes induced by EMT in VM. In addition, the relationship among VM, EMT, CSCs and microenvironment is also discussed briefl y. With the signifi cant part that EMT plays in the formation of VM, a further development of drug for anti-VM formation and a deep-going study of the molecular mechanism of EMT are expected to lay a solid theoretical foundation for the strategies that treatment of tumor distance metastasis by targeting EMT for inhibiting VM formation.

     

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出版历程
  • 收稿日期:  2013-01-30
  • 修回日期:  2013-04-14
  • 刊出日期:  2014-04-24

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