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September 5, 2025Scientific ReportsOpen Access

Combinatorial DNMTs and EZH2 inhibition reprograms the H3K27me3 and DNAme-mediated onco-epigenome to suppress multiple myeloma proliferation

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Authors

APAlba Atienza PárragaPNPatrick NylundKDKlev Diamanti

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Overview

Combinatorial targeting of DNMTs and EZH2 alters DNA methylation and H3K27me3 in multiple myeloma, suggesting a novel therapeutic strategy.

Key Points

  • Combined inhibition of DNMTs and EZH2 significantly suppresses multiple myeloma cell proliferation, inducing apoptosis.
  • Primary multiple myeloma samples exhibited global DNA hypomethylation while specific hypermethylation was found at key gene regulatory regions.
  • Utilizing methods like ChIP-seq and RNA-seq allowed us to document extensive alterations in chromatin states linked to tumor gene activity.
  • These findings highlight the interaction between DNA methylation and H3K27me3 silencing mechanisms in driving cancer progression.

Cite This Study

Párraga et al. (2025) studied this question.

synapsesocial.com/papers/68c2384fb210217d64777613https://doi.org/10.1038/s41598-025-17093-z
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Methylation variability and LINE-1 activation in multiple myeloma2025
  2. 2Methylation variability and LINE-1 transcriptional activation in multiple myeloma2026
  3. 3Dual EZH1/2 inhibition enhances DNMT inhibitor efficacy in colon cancer through targeting H3K27me12025
  4. 4Revealing oncogenic enhancer regulation by epigenomic profiling of multiple myeloma and plasma cell leukemia patient samples2025
  5. 5Unravelling the epigenetic drivers of chip – MDS/CMML – AML progression through novel methylation-sensitive regulatory elements2025