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

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

Author information

1
Institute of Oceanology, Chinese Academy of Sciences, Qingdao, China.

Abstract

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.

PMID:
21264258
PMCID:
PMC3021542
DOI:
10.1371/journal.pone.0016264
[Indexed for MEDLINE]
Free PMC Article

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