ArticleOncogenesis2026
PRMT6-mediated EZH2 arginine methylation is critical for breast cancer development.
Article in Oncogenesis, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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7 authors.
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Abstract
Enhancer of zeste homologue 2 (EZH2), as a key histone methyltransferase, is elevated in multiple malignant tumours, which leads to poor prognosis. However, the underlying mechanisms for mediation of EZH2 enzyme activity remain elusive. Here, we report that PRMT6 asymmetrically dimethylates EZH2 at R509 to promote the bindings between EZH2 and other core component of the polycomb repressive complex 2 (PRC2), which enhances PRC2 induced methylation of histone H3 at K27. EZH2 R509 methylation blocks the expression of PRC2 target genes, leading to breast tumorigenesis in vitro and in vivo. Combination of PRMT6 inhibitor EPZ020411, and EZH2 inhibitor GSK126 effectively suppresses breast tumour growth in the mouse xenografts. Furthermore, immunohistochemical analyses demonstrate there is a positive correlation between PRMT6 and meR509-EZH2 expression in the breast cancer tissues. Consistently, PRMT6 mediated EZH2 R509 methylation is also confirmed in PRMT6-knockout mice. Our findings reveal that PRMT6 inhibitors might be promising combination therapy for EZH2-targeting cancer.
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