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首页> 外文期刊>Oncology Research >MicroRNA-186 Suppresses Cell Proliferation and Metastasis Through Targeting Sentrin-Specific Protease 1 in Renal Cell Carcinoma
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MicroRNA-186 Suppresses Cell Proliferation and Metastasis Through Targeting Sentrin-Specific Protease 1 in Renal Cell Carcinoma

机译：MicroRNA-186通过在肾细胞癌中靶向硒蛋白特异性蛋白酶1来抑制细胞增殖和转移

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摘要

Recent evidence suggests that dysregulation of microRNAs is associated with the development of multiple malignancies. miR-186 has been reported as a critical cancer regulator in several types of cancers. However, its functional significance and molecular mechanism underlying renal cell carcinoma (RCC) remain unknown. In this study, our results showed that miR-186 expression was dramatically downregulated in RCC tissues and cell lines compared to that in adjacent normal tissues and cell lines. Overexpression of miR-186 significantly inhibited cell growth, colony formation, and cell invasion; caused cell cycle arrest at the G(0)/G(1) phase; and induced cell apoptosis as detected by MTT, colony formation, Transwell assay, and flow cytometry assays in RCC cells. In addition, inhibition of miR-186 expression promoted RCC cell proliferation, invasion, and cell cycle progression and reduced apoptosis. Bioinformatics analysis and luciferase reporter assay confirmed that the 3'-UTR of sentrin-specific protease 1 (SENP1) was a direct target of miR-186. A remarkably reverse correlation was observed between miR-186 and SENP1 mRNA in RCC tissues. Furthermore. immunohistochemical staining revealed that SENP1 was positively expressed in RCC specimens. Restoration of SENP1 expression could partially abrogate the inhibitory effect of miR-186 overexpression on RCC cell proliferation through activating NF-KB signaling and its downstream proteins. These data demonstrated that miR-186 acted as a novel tumor suppressor and potential therapeutic biomarker in the progression of RCC by directly targeting SENP1.
机译：最近的证据表明微小RORE测量与多种恶性肿瘤的发展有关。 MiR-186已被报告为几种类型的癌症中作为关键癌症调节剂。然而，其肾细胞癌（RCC）的功能性意义和分子机制仍然未知。在该研究中，我们的结果表明，与相邻的正常组织和细胞系中的相比，MiR-186表达在RCC组织和细胞系中显着下调。 miR-186的过表达显着抑制细胞生长，菌落形成和细胞侵袭;在G（0）/ g（1）相时引起细胞周期停滞;并且由MTT，菌落形成，Transwell测定和RCC细胞中的流式细胞术测定检测的诱导细胞凋亡。此外，抑制miR-186表达促进了RCC细胞增殖，侵袭和细胞周期进展和降低的细胞凋亡。生物信息学分析和荧光素酶报告结果证实，Sentrin特异性蛋白酶1（SeNP1）的3'-UTR是miR-186的直接靶标。在RCC组织中miR-186和SeNP1 mRNA之间观察到显着反向相关性。此外。免疫组织化学染色显示，SENP1在RCC标本中呈正表达。通过激活NF-KB信号传导及其下游蛋白，塞皮1表达的恢复可以部分消除MiR-186过表达对RCC细胞增殖的抑制作用。这些数据证明MIR-186通过直接靶向SENP1，MIR-186作用为新的肿瘤抑制剂和潜在的治疗生物标志物。

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  • 来源
    《Oncology Research》 |2018年第2期|共11页
  • 作者

    Jiao Dan; Wu Man; Ji Lei; Liu Feng; Liu Yingying;

  • 作者单位

    Jilin Univ Dept Ultrasound China Japan Union Hosp Changchun Jilin Peoples R China;

    Jilin Univ Hosp 2 Dept Nephrol Changchun Jilin Peoples R China;

    Changchun Cent Hosp Dept Cardiol Changchun Jilin Peoples R China;

    Jilin Univ China Japan Union Hosp Dept Nephrol 126 Xiantai St Changchun 130033 Jilin Peoples;

    Jilin Univ China Japan Union Hosp Dept Nephrol 126 Xiantai St Changchun 130033 Jilin Peoples;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 肿瘤学;
  • 关键词

    Renal cell carcinoma (RCC); miR-186; SENP1; Proliferation; Tumor suppressor;

    机译：肾细胞癌（RCC）;miR-186;senp1;增殖;肿瘤抑制器;

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