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MiR-30b-5p inhibits proliferation and promotes apoptosis of medulloblastoma cells via targeting MYB proto-oncogene like 2 (MYBL2)
  1. Chengyan Xu,
  2. Zixia He,
  3. Chao Lin,
  4. Zhipeng Shen
  1. Department of Neurosurgery, The Children's Hospital Zhejiang University School of Medicine, National Clinical Research Center For Child Health, Hangzhou, Zhejiang, China
  1. Correspondence to Dr Chengyan Xu, Department of Neurosurgery, The Children's Hospital Zhejiang University School of Medicine, National Clinical Research Center For Child Health, Hangzhou 310000, Zhejiang, China; gujufang2811581558{at}163.com

Abstract

Medulloblastoma (MB) is the most common malignant brain tumors among children. MiR-30b-5p is a potential tumor suppressor in a variety of human cancers. However, its expression and function in MB remain poorly understood. This study aimed to investigate the expression, role and regulatory mechanism of miR-30b-5p in MB. The expression of miR-30b-5p in MB tissues and cell lines was detected by real-time PCR. The effects of miR-30b-5p on cell proliferation and apoptosis were monitored by CCK-8 (Cell Counting Kit-8) assay, colony formation assay and flow cytometry, respectively. Bioinformatics database TargetScan predicted the target genes of miR-30b-5p. The interaction between miR-30b-5p and MYB proto-oncogene Like 2 (MYBL2) was determined by luciferase reporter gene assay. We demonstrated that the expression of miR-30b-5p was significantly downregulated in MB. Upregulated miR-30b-5p could inhibit the proliferation and induce apoptosis of MB.

Moreover, overexpressed miR-30b-5p could increase the expression of BAX but decrease that of Bcl-2. Downregulated miR-30b-5p exerted the opposite effect. MYBL2 was proved to be the target gene of miR-30b-5p and was negatively regulated by miR-30b-5p. These results indicate that miR-30b-5p inhibits the progression of MB via targeting the expression of MYBL2.

  • miR-30b-5p
  • MYBL2
  • medulloblastoma
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Footnotes

  • Contributors Conceived and designed the experiments: CX, ZS. Performed the experiments: CX, ZH, CL, ZS. Statistical analysis: CX. Wrote the paper: CX, ZS. All authors have read and approved the final manuscript.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Patient consent for publication Not required.

  • Ethics approval This study was endorsed by the Ethics Committee of the Children's Hospital affiliated to Medical College of Zhejiang University (approval ID: 201803115).

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Data availability statement Data are available on reasonable request. The data used to support the findings of this study are available from the corresponding author on request.

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