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首页> 外文期刊>Cellular Signalling >LncRNA NEAT1 promotes docetaxel resistance in prostate cancer by regulating ACSL4 via sponging miR-34a-5p and miR-204-5p
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LncRNA NEAT1 promotes docetaxel resistance in prostate cancer by regulating ACSL4 via sponging miR-34a-5p and miR-204-5p

机译：通过冲压miR-34a-5p和miR-204-5p来调节ACSL4，LNCRNA Neat1促进前列腺癌中的多西紫杉醇抗性

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摘要

Docetaxel resistance remains one of the main problems in clinical treatment of metastatic prostate cancer (PCa). Previous studies identified differently expressed lncRNAs in docetaxel-resistant PCa cell lines, while the potential mechanisms were still unknown. In the present study, we found NEAT1 was expressed at high levels in docetaxel-resistant PCa clinical samples and related cell lines. When knockdown NEAT1, cell proliferation and invasion in docetaxel-resistant PCa cells in vitro and in vivo were downregulated. Our further researches explained that NEAT1 exerts oncogenic function in PCa by competitively 'sponging' both miR-34a-5p and miR-204-5p. Inhibition of miR-34a-5p or miR-204-5p expression mimics the docetaxel-resistant activity of NEAT1, whereas ectopic expression of miR-34a-5p or miR-204-5p attenuates the anti-drug function of NEAT1 in PCa cells. Besides, we also found ACSL4 is a target of both miR-34a-5p and miR-204-5p, and ACSL4 was also inhibited by miR-34a-5p and miR-204-5p. Moreover, suppression of miR-34a-5p or/and miR-204-5p greatly restrained the expression of ACSL4 upon NEAT1 overexpression. Joint expression of miR-34a-5p and miR-204a-5p synergistically decreased the expression of ASCL4, indicating miR-34a-5p and miR-204a-5p collaboratively inhibit the expression of ACSL4. Innovatively, we concluded that NEAT1 contributes to the docetaxel resistance by increasing ACSL4 via sponging miR-34a-5p and miR-204-5p in PCa cells.
机译：多西紫杉醇抵抗仍然是转移前列腺癌（PCA）临床治疗中的主要问题之一。以前的研究在多西紫杉醇的PCA细胞系中鉴定了不同表达的LNCRNA，而潜在机制仍然未知。在本研究中，我们发现Neat1在多西紫杉醇抗性PCA临床样本和相关细胞系中以高水平表达。当敲低leat1，体外和体内多西紫杉醇抗性PCA细胞中的细胞增殖和侵袭时被下调。我们的进一步研究解释说，Neat1通过竞争力的“海绵”MIR-34A-5P和MIR-204-5P竞争地区施用PCA致癌功能。抑制miR-34a-5p或miR-204-5p表达模拟了衬垫的多西紫杉型抗性活性，而MiR-34a-5p或miR-204-5p的异位表达衰减PCA细胞中Neat1的抗药物功能。此外，我们还发现ACSL4是MIR-34A-5P和MIR-204-5P的靶标，并且ACSL4也被MIR-34A-5P和MIR-204-5P抑制。此外，抑制miR-34a-5p或/和miR-204-5p的抑制大大抑制了在整齐的过表达时ACSL4的表达。 miR-34a-5p和miR-204a-5p的关节表达协同减少了AsCl4的表达，表明miR-34a-5p和miR-204a-5p协同抑制ACSL4的表达。创新性地，我们得出结论，Neat1通过在PCA细胞中通过海绵MiR-34a-5p和miR-204-5p增加ACSL4来促进多西紫杉醇抗性。

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  • 来源
    《Cellular Signalling》 |2020年第2020期|共8页
  • 作者

    Jiang Xingkang; Guo Shanqi; Zhang Yangyi; Zhao Yang; Li Xiaojiang; Jia Yingjie; Xu Yong; Ma Baojie;

  • 作者单位

    Tianjin Med Univ Dept Urol Hosp 2 Tianjin 300211 Peoples R China;

    Tianjin Univ Tradit Chinese Med Dept Oncol Teaching Hosp 1 Tianjin 300381 Peoples R China;

    Tianjin Med Univ Dept Urol Hosp 2 Tianjin 300211 Peoples R China;

    Tianjin Med Univ Dept Radiol Hosp 2 Tianjin 300211 Peoples R China;

    Tianjin Univ Tradit Chinese Med Dept Oncol Teaching Hosp 1 Tianjin 300381 Peoples R China;

    Tianjin Univ Tradit Chinese Med Dept Oncol Teaching Hosp 1 Tianjin 300381 Peoples R China;

    Tianjin Med Univ Dept Urol Hosp 2 Tianjin 300211 Peoples R China;

    Tianjin Med Univ Dept Urol Hosp 2 Tianjin 300211 Peoples R China;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 细胞形态学;
  • 关键词

    NEAT1; Docetaxel; ACSL4; Prostate cancer; LncRNA;

    机译：Neat1;Docetaxel;ACSL4;前列腺癌;LNCRNA;

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