Role of microRNA-26b in glioma development and its mediated regulation on EphA2

PLoS One. 2011 Jan 14;6(1):e16264. doi: 10.1371/journal.pone.0016264.


Background: MicroRNAs (miRNAs) are short, non-coding RNAs that regulate the expression of multiple target genes. Deregulation of miRNAs is common in human tumorigenesis. Low level expression of miR-26b has been found in glioma cells. However, its underlying mechanism of action has not been determined.

Methodology/principal findings: Real-time PCR was employed to measure the expression level of miR-26b in glioma patients and cells. The level of miR-26b was inversely correlated with the grade of glioma. Ectopic expression of miR-26b inhibited the proliferation, migration and invasion of human glioma cells. A binding site for miR-26b was identified in the 3'UTR of EphA2. Over-expression of miR-26b in glioma cells repressed the endogenous level of EphA2 protein. Vasculogenic mimicry (VM) experiments were performed to further confirm the effects of miR-26b on the regulation of EphA2, and the results showed that miR-26b inhibited the VM processes which regulated by EphA2.

Significance: This study demonstrated that miR-26b may act as a tumor suppressor in glioma and it directly regulates EphA2 expression. EphA2 is a direct target of miR-26b, and the down-regulation of EphA2 mediated by miR-26b is dependent on the binding of miR-26b to a specific response element of microRNA in the 3'UTR region of EphA2 mRNA.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3' Untranslated Regions
  • Binding Sites / genetics
  • Gene Expression Regulation, Neoplastic*
  • Glioma / etiology
  • Glioma / genetics*
  • Glioma / pathology
  • Humans
  • MicroRNAs / physiology*
  • RNA, Messenger / genetics
  • Receptor, EphA2 / genetics*
  • Response Elements / genetics
  • Tumor Suppressor Proteins


  • 3' Untranslated Regions
  • MIRN26A microRNA, human
  • MicroRNAs
  • RNA, Messenger
  • Tumor Suppressor Proteins
  • Receptor, EphA2