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The m6A Reader YTHDF3 Promotes Glioma Progression by Regulating the m6A Modification of lncRNA-PAR5

LiuFei Xu1, Yuan Xu1, YongBin Duan1

  • 1Department of Neurosurgery, First Affiliated Hospital of Kunming Medical University, Kunming, 650000, Yunnan, China, kmmc.cn.

Analytical Cellular Pathology (Amsterdam)
|April 17, 2026
PubMed
Abstract

Insights

The YTHDF3 protein promotes glioma progression by decreasing long non-coding RNA PAR5 (lncRNA-PAR5) levels via m6A modification. Targeting the YTHDF3/PAR5 axis offers a potential therapeutic strategy for glioma.

Area of Science:

  • Oncology
  • Molecular Biology
  • Epigenetics

Background:

  • Glioma progression is inhibited by long non-coding RNA PAR5 (lncRNA-PAR5), which is downregulated in glioma.
  • The precise mechanism behind lncRNA-PAR5 downregulation in glioma remains undetermined.

Purpose of the Study:

  • To elucidate the molecular mechanism of PAR5's tumor-suppressive role in glioma.
  • To investigate the regulatory role of N6-methyladenosine (m6A) modification in PAR5 expression and function.

Main Methods:

  • Bioinformatic prediction of m6A sites in PAR5 and analysis of m6A gene expression in glioblastoma.
  • Experimental validation of YTHDF3 binding to PAR5 and its impact on m6A levels using RNA pull-down, RIP-qPCR, and MeRIP-qPCR.
  • In vitro and in vivo functional assays to assess the roles of PAR5 and YTHDF3 in glioma cell proliferation, invasion, migration, and tumor growth.

Main Results:

  • lncRNA-PAR5 significantly suppressed glioma cell proliferation, invasion, and migration.
  • The m6A reader protein YTHDF3 is upregulated in glioma, binds to PAR5, and enhances its m6A modification, leading to PAR5 degradation and suppressed expression.
  • YTHDF3 knockdown inhibited glioma progression, while YTHDF3 overexpression promoted it; these effects were partially mediated by PAR5 levels. In vivo studies confirmed YTHDF3 knockdown inhibits tumor growth via PAR5 upregulation.

Conclusions:

  • YTHDF3 promotes glioma progression by enhancing m6A modification of PAR5, leading to its degradation.
  • The YTHDF3/PAR5 axis is crucial in glioma development, representing a potential therapeutic target.
Keywords:
YTHDF3gliomainvasionlncRNA-PAR5m6A modificationmigrationproliferation

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