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首页> 外文期刊>Neoplasma: Journal of Experimental and Clinical Oncology >MiR-374b targets GATA3 to promote progression and development of glioblastoma via regulating SEMA3B
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MiR-374b targets GATA3 to promote progression and development of glioblastoma via regulating SEMA3B

机译：miR-374b靶向gata3，促进通过调节sema3b的胶质母细胞瘤的进展和发展

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摘要

In the present study, a series of experiments were conducted to explore the function of miR-374b and the regulatory relationship among miR-374b, GATA3 and SEMA3B in glioma. MiR-374b mimics and inhibitors were employed to regulate miR-374b expression. Besides, qRT-PCR assay was used for detecting the expression level of miR-374b, GATA3 and SEMA3B mRNAs. To verify the targeting relationship between miR-374b and GATA3, dual luciferase analysis was utilized. Moreover, chromatin immunoprecipitation (ChIP) assay was performed to identify the correlation GATA3 with SEMA3B. Furthermore, si1-GATA3, si2-GATA3 and pc-GATA3 were used to regulate GATA3 expression and pc-SEMA3B served for dysregulation the SEMA3B. For assessing the significance of miR374b alone or in co-operation with GATA3 or SEMA3B on cell viability, migration and apoptosis, CCK-8, transwell and FCM assay were also performed. We found that overexpression of miR-374b, which was identified in glioma tissues and cell lines (U251, LN-299 and GOS-3) promoted cell migration and enhanced cell viability but inhibited apoptosis in this study. Furthermore, GATA3 contributed to increase the cell viability and migration and decrease the apoptosis targeted by miR-374b as evidenced by dual luciferase assay. Moreover, GATA3 binding to the promoter of SEMA3B, involved in regulating SEMA3B, was revealed. Further, a series of studies demonstrated that miR-374b targeted GATA3 regulating SEMA3B and resulted in elevation of cell viability and migration but suppressed the apoptosis. However, the promotion effects of miR-374 in glioma process were reversed by co-transfecting pc-GATA3 or pc-SEMA3B. In conclusion, miR-374b promotes glioma process in vitro through suppressing SEMA3B via targeting GATA3. The result of this study provides an important clue to the optimal treatment schedule for glioblastoma.
机译：在本研究中，进行了一系列实验，以探讨miR-374b，miR-374b，gata3和sema3b中的调节关系在胶质瘤中的功能。使用miR-374b模拟物和抑制剂来调节miR-374b表达。此外，QRT-PCR测定用于检测miR-374b，gata3和sema3b mRNA的表达水平。为了验证miR-374b和gata3之间的靶向关系，使用了双荧光素酶分析。此外，进行染色质免疫沉淀（芯片）测定以鉴定用SEMA3B鉴定相关性GATA3。此外，Si1-GATA3，Si2-GATA3和PC-GATA3用于调节GATA3表达，PC-SEMA3B用于SEMA3B的呼吸困难。为了评估单独的miR374b的重要性或在细胞活力上与GATA3或SEMA3b进行协同操作，还进行了迁移和细胞凋亡，CCK-8，Transwell和FCM测定。我们发现miR-374b的过表达，其在胶质瘤组织和细胞系（U251，LN-299和GOS-3）中鉴定出促进细胞迁移和增强的细胞活力，但抑制了该研究的细胞凋亡。此外，GATA3有助于增加细胞活力和迁移，并降低MIR-374b靶向的细胞凋亡，如双荧光素酶测定所证明的。此外，揭示了与参与调节SEMA3B的SEMA3B的启动子的GATA3结合。此外，一系列研究证明了MiR-374b靶向GATA3调节SEMA3B，并导致细胞活力和迁移升高，但抑制了凋亡。然而，通过共转染PC-GATA3或PC-SEMA3B，逆转MIR-374在胶质瘤过程中的促进效应。总之，MIR-374B通过靶向GATA3抑制SEMA3B，促进胶质瘤过程。本研究的结果为胶质母细胞瘤的最佳治疗时间表提供了重要的线索。

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  • 作者

    Gao J.; Bai S.; Wang Y.; Zhao S.; He Z.; Wang R.;

  • 作者单位

    Inner Mongolia Med Univ Affiliated Hosp Dept Image Diagnost Hohhot Peoples R China;

    Inner Mongolia Med Univ Affiliated Hosp Dept Dermatol Hohhot Peoples R China;

    Inner Mongolia Med Univ Affiliated Hosp Dept Clin Lab Hohhot Peoples R China;

    Inner Mongolia Med Univ Affiliated Hosp Dept Image Diagnost Hohhot Peoples R China;

    Inner Mongolia Med Univ Affiliated Hosp Dept Neurosurg Hohhot Peoples R China;

    Inner Mongolia Med Univ Affiliated Hosp Dept Image Diagnost Hohhot Peoples R China;

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

    miR-374b; glioma; U251; GATA3; SEMA3B;

    机译：MER-374 B;GLIM;1;

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