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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Essential role of Stat3 in PI3K-induced oncogenic transformation
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Essential role of Stat3 in PI3K-induced oncogenic transformation

机译：Stat3在PI3K致癌性转化中的重要作用

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摘要

Cells transformed by the p110a-H1047R mutant of PI3K show increased tyrosine phosphorylation of Stat3. This activation of Stat3 is important for the transformation process, because a dominant-negative mutant of Stat3 interferes with PI3K-induced oncogene-sis. GDC-0941, a specific inhibitor of PI3K reduces the level of Stat3 phosphorylation. The effect of PI3K on Stat3 appears to be mediated by a member of the Tec kinase family. The Tec kinase inhibitor LFM-A13 blocks Stat3 phosphorylation in H1047R-transformed cells. The Janus kinase inhibitor AG490 and the Src kinase inhibitor Src-1, as well as rapamycin, have no effect on Stat3 phosphorylation in H1047R-transformed cells. The H1047R-transformed cells also release a factor that induces Stat3 phosphorylation in normal cells with possible effects on the cellular microenvironment. In some human tumor cell lines, the enhanced phosphorylation of Stat3 is inhibited by both PI3K and by Tec kinase inhibitors, suggesting that the link between PI3K and Stat3 is significant in human cancer.
机译：由PI3K的p110a-H1047R突变体转化的细胞显示出Stat3的酪氨酸磷酸化增加。 Stat3的这种激活对于转化过程非常重要，因为Stat3的显性负突变会干扰PI3K诱导的癌基因的产生。 GDC-0941是PI3K的特异性抑制剂，可降低Stat3磷酸化水平。 PI3K对Stat3的作用似乎是由Tec激酶家族的成员介导的。 Tec激酶抑制剂LFM-A13在H1047R转化的细胞中阻断Stat3磷酸化。 Janus激酶抑制剂AG490和Src激酶抑制剂Src-1以及雷帕霉素对H1047R转化细胞中的Stat3磷酸化没有影响。 H1047R转化的细胞还释放出一种因子，该因子可诱导正常细胞中的Stat3磷酸化，并可能对细胞微环境产生影响。在一些人类肿瘤细胞系中，Stat3的磷酸化增强受到PI3K和Tec激酶抑制剂的抑制，这表明PI3K和Stat3之间的联系在人类癌症中很重要。

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  • 作者

    Jonathan R. Hart; Lujian Liao; John R. Yates lll; Peter K. Vogt;

  • 作者单位

    Department of Molecular and Experimental Medicine and bDepartment of Chemical Physiology, The Scripps Research Institute, La Jolla, CA 92037;

    Department of Molecular and Experimental Medicine and bDepartment of Chemical Physiology, The Scripps Research Institute, La Jolla, CA 92037;

    Department of Molecular and Experimental Medicine and bDepartment of Chemical Physiology, The Scripps Research Institute, La Jolla, CA 92037;

    Department of Molecular and Experimental Medicine and bDepartment of Chemical Physiology, The Scripps Research Institute, La Jolla, CA 92037;

  • 收录信息 美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
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  • 关键词

    oncogenic signaling; tumor stroma; tyrosine kinase;

    机译：致癌信号;肿瘤基质;酪氨酸激酶;

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