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首页> 外文期刊>Cell biology international. >Lysophosphatidic acid modulates the association of PTP1B with N-cadherin/catenin complex in SKOV3 ovarian cancer cells
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Lysophosphatidic acid modulates the association of PTP1B with N-cadherin/catenin complex in SKOV3 ovarian cancer cells

机译：溶血膦酸在skov3卵巢癌细胞中用n-cadherin / catenin复合物调节ptp1b的关联

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摘要

LPA (lysophosphatidic acid) is a natural phospholipid that plays important roles in promoting cancer cell proliferation, invasion and metastases. We previously reported that LPA induces ovarian cancer cell dispersal and disruption of AJ (adherens junction) through the activation of SFK (Src family kinases). In this study, we have investigated the regulatory mechanisms during the early phase of LPA-induced cell dispersal. An in vitro model of the ovarian cancer cell line SKOV3 for cell dispersal was used. LPA induces rapid AJ disruption by increasing the internalization of N-cadherin-β-catenin. By using immunoprecipitations, LPA was shown to induce increased tyrosine phosphorylation of β-catenin and alter the balance of β-catenin-bound SFK and PTP1B (phosphotyrosine phosphatase 1B). The altered balance of tyrosine kinase/phosphatase correlated with a concomitant disintegration of the β-catenin-α-catenin, but not the β-catenin-N-cadherin complex. This disintegration of β-catenin from α-catenin and the cell dispersal caused by LPA can be rescued by blocking SFK activity with the chemical inhibitor, PP2. More importantly, PP2 also restores the level of PTP1B bound to β-catenin. We propose that LPA signalling alters AJ stability by changing the dynamics of tyrosine kinase/phosphatase bound to AJ proteins. This work provides further understanding of the early signalling events regulating ovarian cancer cell dispersal and AJ disruption induced by LPA.
机译：LPA（溶血磷脂酸）是一种天然磷脂，可在促进癌细胞增殖，侵袭和转移方面发挥重要作用。我们之前报道，LPA通过SFK（SRC Family Kinases）的激活诱导卵巢癌细胞分散和AJ（粘附结）的破坏。在这项研究中，我们在LPA诱导的细胞分散期期间调查了调节机制。使用卵巢癌细胞系Skov3的体外模型用于细胞分散。 LPA通过增加N-cadherin-β-catenin的内化诱导快速的AJ破坏。通过使用免疫沉淀，显示LPA诱导β-连环蛋白的酪氨酸磷酸化增加，并改变β-连环蛋白结合的SFK和PTP1B的平衡（磷酸酪氨酸磷酸酶1B）。酪氨酸激酶/磷酸酶的改变与β-连环蛋白-α-连环蛋白的伴随崩解相关，但不是β-连环蛋白-N-钙粘蛋白复合物相关。通过将SFK活性与化学抑制剂，PP2阻断SFK活性，可以抵抗来自α-catenin的β-catenin的这种崩解和由LPA引起的细胞分散液进行崩解。更重要的是，PP2还恢复与β-catenin结合的PTP1b水平。我们提出LPA信号传导通过改变与AJ蛋白结合的酪氨酸激酶/磷酸酶的动态改变AJ稳定性。这项工作提供了对调节LPA诱导的卵巢癌细胞分散和AJ破坏的早期信号传导事件进一步了解。

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  • 来源
    《Cell biology international.》 |2012年第9期|共9页
  • 作者

    HuangR.Y.; WenC.-C.; LiaoC.-K.; WangS.-H.; ChouL.-Y.; WuJ.-C.;

  • 作者单位

    Department of Obstetrics and Gynaecology National University Hospital of Singapore Singapore;

    Department of Anatomy and Cell Biology College of Medicine National Taiwan University Taipei;

    Department of Anatomy and Cell Biology College of Medicine National Taiwan University Taipei;

    Department of Anatomy and Cell Biology College of Medicine National Taiwan University Taipei;

    Department of Anatomy and Cell Biology College of Medicine National Yang-Ming University Taipei;

    Department of Anatomy and Cell Biology College of Medicine National Yang-Ming University Taipei;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 细胞生物学;
  • 关键词

    Adherens junction; Lpa; Ovarian cancer; Ptp1b; Src; Tyrosine kinase;

    机译：粘附结;LPA;卵巢癌;ptp1b;src;酪氨酸激酶;

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