Long Non-Coding RNA MEG3 Modifies Cell-Cycle, Migration, Invasion, and Proliferation Through AKAP12 by Sponging...

Area of Science:

• Neuro-oncology
• Molecular Biology
• Gene Regulation

Background:

• Meningioma (MEN) is a prevalent central nervous system tumor.
• Long non-coding RNA maternally expressed gene 3 (MEG3) is implicated in MEN progression.
• The precise mechanisms by which MEG3 influences MEN aggressiveness require further elucidation.

Purpose of the Study:

• To investigate the molecular mechanisms underlying the role of MEG3 in regulating the aggressive phenotypes of meningioma.
• To explore the interaction between MEG3, microRNA-29c (miR-29c), and A-kinase anchor protein 12 (AKAP12) in MEN cells.

Main Methods:

• Quantitative real-time Polymerase Chain Reaction (qRT-PCR) for gene expression analysis.
• Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays to confirm molecular interactions.
• Western blot for protein level detection.
• Functional assays including cell-cycle analysis, wound healing, Transwell invasion, and CCK-8 assays to assess cellular behavior.

Main Results:

• MEG3 and AKAP12 expression were downregulated, while miR-29c was upregulated in MEN tissues and cell lines.
• MEG3 acted as a molecular sponge for miR-29c, thereby regulating AKAP12 expression.
• Overexpression of MEG3 inhibited cell-cycle progression, migration, invasion, and proliferation in MEN cells, effects reversed by miR-29c.
• AKAP12 depletion counteracted the inhibitory effects of miR-29c inhibition on MEN cell behaviors.

Conclusions:

• MEG3 exerts its tumor-suppressive functions in meningioma via the miR-29c/AKAP12 axis.
• The MEG3/miR-29c/AKAP12 pathway is crucial in mediating the aggressive behaviors of MEN cells.
• MEG3 demonstrates potential as a biomarker for meningioma diagnosis and therapeutic intervention.