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mir-218-2 promotes glioblastomas growth, invasion and drug resistance by targeting CDC27

Zhuoying Feng1, Luping Zhang1, Junchen Zhou1

  • 1Institute of Human Anatomy and Histology and Embryology, Otology & Neuroscience Center, Binzhou Medical University, Laishan District, Shandong Province, 264003,China.

Oncotarget
|December 16, 2016
PubMed

Insights

MicroRNA-218-2 (mir-218-2) is overexpressed in glioma and promotes tumor growth, invasion, and migration. Inhibiting mir-218-2 could be a potential therapeutic strategy for glioma.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Glioma is a major cause of cancer morbidity and mortality worldwide.
  • Understanding glioma's molecular mechanisms is crucial for developing effective treatments.
  • MicroRNAs (miRNAs) are increasingly recognized for their roles in cancer, with mir-218 identified as an anti-oncogene, but specific isoforms like mir-218-2 require further investigation.

Purpose of the Study:

  • To investigate the specific role and function of microRNA-218-2 (mir-218-2) in glioma.
  • To determine the correlation between mir-218-2 expression and glioma cell behavior.
  • To identify downstream targets of mir-218-2 involved in glioma regulation.

Main Methods:

  • Quantitative real-time PCR to assess mir-218-2 expression levels in glioma tissues and cells.
  • In vitro assays (proliferation, invasion, migration) to evaluate the effects of mir-218-2 overexpression and inhibition.
  • In vivo studies using xenograft models to assess the impact of mir-218-2 on tumor growth.
  • Western blotting and luciferase reporter assays to validate Cell Division Cycle 27 (CDC27) as a downstream target of mir-218-2.

Main Results:

  • MicroRNA-218-2 (mir-218-2) was found to be significantly overexpressed in glioma.
  • Overexpression of mir-218-2 promoted glioma cell proliferation, invasion, and migration in vitro.
  • In vivo, mir-218-2 overexpression led to increased glioma tumor growth.
  • mir-218-2 expression positively correlated with glioma cell drug susceptibility to β-lapachone.
  • Cell Division Cycle 27 (CDC27) was identified as a direct downstream target of mir-218-2, and its overexpression counteracted mir-218-2's effects.

Conclusions:

  • MicroRNA-218-2 (mir-218-2) acts as an oncogene in glioma, promoting tumor progression.
  • The oncogenic function of mir-218-2 is mediated, in part, through its regulation of CDC27.
  • These findings highlight mir-218-2 as a potential therapeutic target for glioma treatment.
Keywords:
CDC27gliomasinvasionmir-218-2proliferation

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