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首页> 外文期刊>Cell cycle >CASC15 contributes to proliferation and invasion through regulating miR-766-5p/ KLK12 axis in lung cancer
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CASC15 contributes to proliferation and invasion through regulating miR-766-5p/ KLK12 axis in lung cancer

机译：CASC15通过调节肺癌中的miR-766-5p / klk12轴来促进增殖和侵袭

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摘要

Long non-coding RNAs (lncRNAs) are key mediators of cancer. The dysregulation of a lncRNA, CASC15, has been linked to several cancers, except lung cancer. Here, the aim of the study was to explore the role and mechanism of CASC15 in lung cancer regulation, with the focus on its interaction with a potential target, microRNA-766-5p (miR-766-5p) and an oncogene, kallikrein-related peptidase 12 (KLK12). Quantitative real-time PCR (qRT-PCR) was used to assess levels of CASC15, miR-766-5p and KLK12 in lung cancer tissues or cells. Western blot analysis was used to detect KLK12 protein expression. Ectopic expression of CASC15 was induced by a lentiviral system. CCK-8 and transwell assays were used to evaluate lung cancer cell proliferation and invasion, respectively. The interaction among CASC15, miR-766-5p and KLK12 was investigated by bioinformatical analysis and luciferase assay. In lung cancer tissue and cells, CASC15 was upregulated, while miR-766-5p was downregulated. Overexpression of CASC15 promoted lung cancer cell proliferation and invasion. A negative correlation was found between CASC15 and miR-766-5p levels. Overexpression of miR-766-6p reversed the cancer-promoting role of CASC15 in lung cancer cells, which was mediated by KLK12. The tumor-promoting role of CASC15 and tumor-suppressing role of miR-766-5p were also validated in vivo in tumor bearing mice, and KLK12 was also shown as an important mediator. CASC15 promotes lung cancer through the miR-766-5p/KLK12 axis, indicating that CASC15 is a potential therapeutic in lung cancer.
机译：长期非编码RNA（LNCRNA）是癌症的关键介质。除了肺癌之外，LNCrNA的失调Casc15 Casc15已与几种癌症相关联。在这里，该研究的目的是探讨Casc15在肺癌调节中的作用和机制，重点关注其与潜在目标的相互作用，MicroRNA-766-5P（miR-766-5p）和癌基因kallikrein-相关肽酶12（KLK12）。定量实时PCR（QRT-PCR）用于评估肺癌组织或细胞中Casc15，miR-766-5p和Klk12的水平。 Western印迹分析用于检测KLK12蛋白表达。 Casc15的异位表达由慢病毒系统诱导。 CCK-8和Transwell测定分别用于评估肺癌细胞增殖和侵袭。通过生物信息分析和荧光素酶测定研究了CASC15，MIR-766-5P和KLK12之间的相互作用。在肺癌组织和细胞中，Casc15被上调，而MiR-766-5P下调。 Casc15的过度表达促进了肺癌细胞增殖和侵袭。 Casc15和MiR-766-5P水平之间发现了负相关性。 MiR-766-6P的过度表达逆转了Casc15在肺癌细胞中的癌症促进作用，该肺癌细胞由KLK12介导。 Casc15的肿瘤促进作用和miR-766-5p的肿瘤抑制作用也在肿瘤轴承小鼠体内验证，并且KLK12也显示为重要的介体。 Casc15通过MiR-766-5P / KLK12轴促进肺癌，表明Casc15是肺癌的潜在治疗性。

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  • 来源
    《Cell cycle》 |2019年第18期|共9页
  • 作者

    Bai Yong; Zhang Guojun; Cheng Ruirui; Yang Rui; Chu Heying;

  • 作者单位

    Zhengzhou Univ Dept Resp Affiliated Hosp 1 Zhengzhou Henan Peoples R China;

    Zhengzhou Univ Dept Resp Affiliated Hosp 1 Zhengzhou Henan Peoples R China;

    Zhengzhou Univ Dept Resp Affiliated Hosp 1 Zhengzhou Henan Peoples R China;

    Zhengzhou Univ Dept Resp Affiliated Hosp 1 Zhengzhou Henan Peoples R China;

    Zhengzhou Univ Dept Resp Affiliated Hosp 1 Zhengzhou Henan Peoples R China;

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

    Lung cancer; CASC15; miR-766-5p; KLK12;

    机译：肺癌;Casc15;WE-766-5P;CLK12;

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