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首页> 外文期刊>Science Signaling >The IncRNA HI9 mediates breast cancer cell plasticity during EMT and MET plasticity by differentially sponging miR-200b/c and let-7b
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The IncRNA HI9 mediates breast cancer cell plasticity during EMT and MET plasticity by differentially sponging miR-200b/c and let-7b

机译：Incrna Hi9在EMT期间介导乳腺癌细胞可塑性，并通过差异的海绵miR-200b / c和let-7b来满足可塑性

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摘要

Metastasis is a multistep process by which tumor cells disseminate from their primary site and form secondary tumors at a distant site. The pathophysiological course of metastasis is mediated by the dynamic plasticity of cancer cells, which enables them to shift between epithelial and mesenchymal phenotypes through a transcriptionally regulated program termed epithelial-to-mesenchymal transition (EMT) and its reverse process, mesenchymal-to-epithelial transition (MET). Using a mouse model of spontaneous metastatic breast cancer, we investigated the molecular mediators of metastatic competence within a heterogeneous primary tumor and how these cells then manipulated their epithelial-mesenchymal plasticity during the metastatic process. We isolated cells from the primary mammary tumor, the circulation, and metastatic lesions in the lung in TA2 mice and found that the long noncoding RNA (IncRNA) H19 mediated EMT and MET by differentially acting as a sponge for the microRNAs miR-200b/c and let-7b. We found that this ability enabled HI9 to modulate the expression of the microRNA targets G/f2 and Cyth3, respectively, which encode regulators of the RAS superfamily member adenosine 5'-diphosphate (ADP) ribosylation factor (ARF), a gua-nosine triphosphatase (GTPase) that promotes cell migration associated with EMT and disseminating tumor cells. Decreasing the abundance of H19 or manipulating that of members in its axis prevented metastasis from grafts in syngeneic mice. Abundance of H19, GIT2, and CYTH3 in patient samples further suggests that H19 might be exploited as a biomarker for metastatic cells within breast tumors and perhaps as a therapeutic target to prevent metastasis.
机译：转移是一种多步骤过程，通过该过程，肿瘤细胞从其主要部位散发并在远处部位形成次级肿瘤。转移的病理生理学过程是由癌细胞的动态可塑性介导的，这使得它们通过转录调节的程序被称为上皮 - 间充质转换（EMT）的上皮和间充质表型转化及其反向过程，间充质 - 上皮过渡（遇见）。使用自发性转移性乳腺癌的小鼠模型，我们研究了在异质原发性肿瘤内的转移能力的分子介质以及这些细胞在转移过程中如何操纵它们的上皮 - 间充质可塑性。从TA2小鼠中肺部中的循环和转移性病变中分离出细胞，发现长度非编码RNA（IncRNA）H19介导的EMT并通过差异作用为MicroRNA MiR-200b / c的海绵。和let-7b。我们发现这种能力使HI9分别调节MicroRNA靶G / F2和Cyth3的表达，其编码RAS超家族成员腺苷5'-二磷酸（ADP）核糖基化因子（ARF）的稳压器，GUA-鼻鼻磷酸盐酶（GTP酶）促进与EMT和促进肿瘤细胞相关的细胞迁移。降低H19的丰度或操纵其轴中的成员的成员，以防止来自同工小鼠的移植物中的转移。患者样品中的H19，GIT2和Cyth3的丰度进一步表明H19可能被利用为乳腺肿瘤内转移细胞的生物标志物，并且可能是预防转移的治疗靶标。

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  • 来源
    《Science Signaling》 |2017年第483期|共10页
  • 作者

    Wu Zhou; Xiao-lei Ye; Jun Xu; Ming-Guo Cao; Zheng-Yu Fang; Ling-Yun Li; Guang-Hui Guan; Qiong Liu; Yue-Hui Qian; Dong Xie;

  • 作者单位

    Department of Medicine College of Medicine and Health Lishui University Zhejiang 323000 China;

    Division of Drugs and Pharmacology Ningbo Institute of Medical Sciences Zhejiang 315020 China;

    Department of Medicine College of Medicine and Health Lishui University Zhejiang 323000 China;

    Department of Medicine College of Medicine and Health Lishui University Zhejiang 323000 China;

    Department of Medicine College of Medicine and Health Lishui University Zhejiang 323000 China;

    Laboratory of Medicine People's Hospital of Lishui City Lishui 323000 China;

    Division of Drugs and Pharmacology Ningbo Institute of Medical Sciences Zhejiang 315020 China;

    Division of Drugs and Pharmacology Ningbo Institute of Medical Sciences Zhejiang 315020 China;

    Department of Laboratory Animal Science Tianjin Medical University Tianjin 300007 China;

    Institute for Nutritional Sciences Shanghai Institutes for Biological Sciences Chinese Academy of Sciences Shanghai 200031 China.;

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  • 正文语种 eng
  • 中图分类 细胞生物学;
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