LINC00511 knockdown suppresses glioma cell malignant progression through miR-15a-5p/AEBP1 axis

Zhen Liu1, Bei Tao2, Linkun Li1

  • 1Neurosurgery Department, Nanyang Second General Hospital, China.

Abstract

Insights

Long intergenic non-protein coding RNA 511 (LINC00511) promotes glioma progression. Knocking down LINC00511 inhibits glioma cell viability, migration, and invasion through the miR-15a-5p/AEBP1 pathway.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • A known association exists between long intergenic non-protein coding RNA 511 (LINC00511) and glioma.
  • The precise mechanism by which LINC00511 influences glioma remains unclear.

Purpose of the Study:

  • To elucidate the underlying mechanism of LINC00511 in glioma progression.
  • To investigate the role of LINC00511 in regulating glioma cell biological characteristics.

Main Methods:

  • Quantitative real-time PCR (RT-qPCR) and bioinformatics analyses were used to determine LINC00511 expression in glioma.
  • Dual-luciferase assays verified the interaction between LINC00511 and miR-15a-5p.
  • In vitro and in vivo experiments, including cell transfection, rescue assays, and tumorigenesis assays, were performed to assess the functional impact of LINC00511 knockdown and the miR-15a-5p/AEBP1 axis.

Main Results:

  • LINC00511 was found to be upregulated in glioma tissues.
  • LINC00511 knockdown suppressed glioma cell viability, proliferation, migration, invasion, and induced apoptosis.
  • The study identified a regulatory axis where LINC00511 influences glioma progression via sponging miR-15a-5p, which targets AEBP1, subsequently affecting p65 phosphorylation and epithelial-mesenchymal transition (EMT).

Conclusions:

  • LINC00511 knockdown inhibits glioma cell progression by regulating the miR-15a-5p/AEBP1 axis.
  • LINC00511 acts as a potential oncogene in glioma, suggesting therapeutic targeting of this axis.

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