ArticleJournal of neuro-oncology2026
The MALAT1-EZH2 axis regulates PRC2 activity and promotes the mesenchymal phenotype in pediatric atypical teratoid/rhabdoid tumors.
Article in Journal of neuro-oncology, 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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Who cites it
1 citing paper in PubMed.
- Clinicopathological Characterization of Pediatric Atypical Teratoid/Rhabdoid Tumors and an HE-IHC Dual-Path Deep Learning Model for Auxiliary Diagnosis.Diagnostics (Basel, Switzerland) · 2026Article
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17 authors.
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Abstract
backgroundAtypical teratoid/rhabdoid tumors (AT/RT) are aggressive pediatric CNS malignancies characterized by SMARCB1 loss, which leads to the dysregulated expression of Enhancer of Zeste Homolog 2 (EZH2), a key catalytic component of the Polycomb Repressive Complex 2 (PRC2). This dysregulation results in aberrant trimethylation of histone H3 at lysine 27 (H3K27me3), driving tumor progression. While EZH2 inhibitors like tazemetostat are in clinical use, their efficacy remains limited, necessitating a deeper understanding of PRC2 regulation. We investigated the role of long non-coding RNAs (lncRNAs) in modulating the EZH2-PRC2 axis in AT/RT.
methodsExpression levels of lncRNAs (MALAT1, ANRIL, KCNQ1OT1) were analyzed via RT-PCR in 10 archival AT/RT patient tissues. RNA immunoprecipitation (RIP) was performed to identify direct interactions with EZH2. The functional impact of MALAT1 inhibition on H3K27me3 levels, mesenchymal markers (CDH2, TWIST, ZEB1), and tumorigenic behaviors (migration, invasion, sphere formation) was evaluated in vitro.
resultsMALAT1, ANRIL, and KCNQ1OT1 were significantly overexpressed in AT/RT tissues (p < 0.05). RIP assays revealed that only MALAT1 directly interacts with EZH2 in DAOY and primary AT/RT cells. MALAT1 knockdown significantly reduced H3K27me3 levels (p < 0.05) and markedly impaired cell migration, invasion, and sphere-forming capacity. These phenotypic changes were associated with the downregulation of key mesenchymal markers (CDH2, TWIST, ZEB1).
conclusionsOur findings identify MALAT1 as a critical epigenetic regulator in AT/RT that interacts with EZH2 to maintain the PRC2-mediated repressive landscape. Targeting the MALAT1-EZH2 axis provides a novel translational perspective to enhance the efficacy of epigenetic therapies in AT/RT.
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