MicroRNA-181 inhibits glioblastoma cell growth by directly targeting CCL8

Fengyu Zhai1,2, Xinfeng Chen1,3, Qianyi He4

  • 1Biotherapy Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, P.R. China.

Oncology Letters
|August 20, 2019
PubMed

Insights

MicroRNA-181 (miR-181) is downregulated in glioblastoma, hindering tumor growth and progression. Restoring miR-181 levels shows therapeutic potential for glioblastoma treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • MicroRNAs (miRNAs) play crucial roles in cancer development.
  • The specific function of miR-181 in glioblastoma remains unclear.
  • Glioblastoma is an aggressive brain tumor with limited treatment options.

Purpose of the Study:

  • To investigate the role of miR-181 in glioblastoma.
  • To determine the molecular mechanisms underlying miR-181's function.
  • To evaluate miR-181 as a potential therapeutic target.

Main Methods:

  • Analysis of miR-181 expression in glioblastoma tissues and cell lines.
  • Overexpression of miR-181 in glioblastoma cells.
  • Assessment of cell proliferation, invasion, migration, cell cycle, and apoptosis.
  • Luciferase reporter assays to confirm direct interaction between miR-181 and CCL8.
  • Overexpression of C-C motif chemokine ligand 8 (CCL8) to reverse miR-181 effects.

Main Results:

  • miR-181 was significantly downregulated in glioblastoma tissues and cell lines.
  • Low miR-181 expression correlated with poor patient prognosis.
  • miR-181 overexpression suppressed glioblastoma cell proliferation, invasion, and migration.
  • miR-181 induced cell cycle arrest at G1 phase and promoted apoptosis.
  • miR-181 directly targeted and reduced CCL8 expression.
  • CCL8 was upregulated in glioblastoma and its effects were opposite to miR-181.

Conclusions:

  • miR-181 acts as a tumor suppressor in glioblastoma.
  • The miR-181/CCL8 axis is a key regulator of glioblastoma progression.
  • miR-181 is a promising molecular biomarker and therapeutic target for glioblastoma.

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