ArticleAnalytical cellular pathology (Amsterdam)2026
The m6A Reader YTHDF3 Promotes Glioma Progression by Regulating the m6A Modification of lncRNA-PAR5.
Article in Analytical cellular pathology (Amsterdam), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- The m6A Reader YTHDF3 Promotes Glioma Progression by Regulating the m6A Modification of lncRNA-PAR5.Analytical cellular pathology (Amsterdam) · 2026Article
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6 authors.
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Abstract
backgroundLong non-coding RNA PAR5 (lncRNA-PAR5) is downregulated in glioma and has been confirmed to inhibit glioma progression; however, the specific regulatory mechanism underlying its downregulation remains unclear.
objectiveThis study aimed to investigate the key molecular mechanism by which PAR5 inhibits glioma progression, with a focus on the regulatory role of m6A modification.
methodsPotential m6A modification sites in the PAR5 sequence were predicted using the SRAMP online tool. The expression profiles of m6A regulatory genes in glioblastoma were analyzed via the GEPIA database. RNA pull-down, RIP-qPCR, and MeRIP-qPCR were employed to validate the specific binding of YTHDF3 to PAR5 and its effect on the m6A modification level of PAR5. The expression of PAR5 and YTHDF3 was modulated by cell transfection, and cell proliferation, invasion, and migration were assessed using CCK-8, Transwell, and wound healing assays, respectively. Further in vivo functional validation was performed using a subcutaneous xenograft tumor model in nude mice.
resultslncRNA-PAR5 significantly inhibited the proliferation, invasion, and migration of glioma cells. Bioinformatics analysis and experimental validation revealed that the m6A reader protein YTHDF3 is highly expressed in glioma, specifically recognizes and binds to PAR5, and promotes PAR5 degradation by enhancing its m6A modification level, thereby negatively regulating PAR5 expression. Functional experiments demonstrated that YTHDF3 plays a pro‑oncogenic role, while knockdown of YTHDF3 suppressed malignant phenotypes of glioma, an effect that could be partially reversed by simultaneous knockdown of PAR5. In vivo experiments further confirmed that YTHDF3 knockdown inhibits tumor growth by upregulating PAR5.
conclusionYTHDF3 promotes glioma cell proliferation, invasion, and migration by inhibiting PAR5 expression through enhancing its m6A modification. This study reveals the critical role of the YTHDF3/PAR5 axis in glioma progression and provides a potential novel target for glioma‑targeted therapy.
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