MicroRNA-505-3p inhibits development of glioma by targeting HMGB1 and regulating AKT expression

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Characterization of Functionally Associated miRNAs in Glioblastoma and their Engineering into Artificial Clusters for Gene Therapy
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Characterization of Functionally Associated miRNAs in Glioblastoma and their Engineering into Artificial Clusters for Gene Therapy

Published on: October 4, 2019

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Zhenlin Cheng1, Bin Wang1, Cheng Zhang2

  • 1Department of Neurosurgery, Zhangye People's Hospital Affiliated to Hexi University, Zhangye, Gansu 734000, P.R. China.

Oncology Letters
|July 30, 2020
PubMed

Insights

MicroRNA-505-3p is reduced in glioma, suppressing tumor growth by targeting High-Mobility Group Box 1 (HMGB1). This microRNA inhibits glioma cell proliferation, migration, and invasion.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • MicroRNA (miR)-505 has a known role in human cancers.
  • The specific regulatory mechanism of the miR-505-3p/High-Mobility Group Box 1 (HMGB1) axis in glioma remains largely unelucidated.
  • Understanding this axis is crucial for developing novel glioma therapies.

Purpose of the Study:

  • To elucidate the regulatory mechanism of the miR-505-3p/HMGB1 axis in glioma.
  • To investigate the functional role of miR-505-3p in glioma progression.
  • To determine if HMGB1 is a direct target of miR-505-3p in glioma.

Main Methods:

  • Quantitative real-time PCR (RT-qPCR) for miR-505-3p and HMGB1 expression.
  • Western blot analysis for protein expression.
  • Dual luciferase assay to confirm miR-505-3p and HMGB1 interaction.
  • MTT and Transwell assays to assess cell proliferation, migration, and invasion.

Main Results:

  • miR-505-3p expression was significantly decreased in glioma tissues, correlating with poor clinical outcomes.
  • Overexpression of miR-505-3p inhibited glioma cell proliferation, migration, and invasion.
  • HMGB1 was identified as a direct target of miR-505-3p.
  • miR-505-3p suppressed epithelial-mesenchymal transition (EMT) by inhibiting p-AKT expression.

Conclusions:

  • miR-505-3p inhibits glioma development by directly targeting HMGB1.
  • The miR-505-3p/HMGB1 axis plays a critical role in regulating glioma cell behavior.
  • miR-505-3p exerts its tumor-suppressive effects partly through the regulation of AKT signaling and EMT.
Keywords:
AKTHMGB1gliomamiR-505-3p

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