ArticleScientific reports2025
Combinatorial DNMTs and EZH2 inhibition reprograms the H3K27me3 and DNAme-mediated onco-epigenome to suppress multiple myeloma proliferation.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Concurrent Remission of Therapy-Related Acute Myeloid Leukemia and IgG-λ MGUS During Oral Decitabine-Cedazuridine: A Case Report.Hematology reports · 2026Article
- N-Azacytidine Inhibits Myeloma Cell Growth While Preserving Multiple Myeloma Patient Derived-Bone Marrow Mesenchymal Stromal Cells Differentiation.Metabolites · 2026Article
- Deciphering epigenetic crosstalk in multiple myeloma pathogenesis and treatment.Clinical epigenetics · 2026Review
- Epigenetic mechanisms of drug resistance in acute myeloid leukemia: advances in small-molecule targeted therapy.Frontiers in pharmacology · 2025Review
- CRISPR-epigenetic crosstalk: From bidirectional regulation to therapeutic potential.Computational and structural biotechnology journal · 2025Review
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Authors and funding
17 authors.
Funding
Abstract
Comprehensive epigenomic studies in multiple myeloma (MM) that unravel the connections between major epigenetic regulators, their intertwined collaboration and the potential of combinatorial targeting remain limited. Utilizing ChIP-seq, ATAC-seq, RNA-seq, and DNA methylation (DNAme) data, we generated whole-genome chromatin annotations from normal plasma cells and MM patients, revealing epigenomic re-configuration affecting downstream genes involved in tumour growth and survival. Primary MM samples showed global DNA hypomethylation but site-specific hypermethylation was observed at transcription start sites, promoters, and enhancers. Moreover, increased deposition of H3K27me3 was observed in clinically relevant functional chromatin clusters. Combined EZH2 and DNMTs inhibition resulted in extensive epigenomic alterations activating apoptosis and cell cycle genes, leading to increased G2/M arrest and apoptosis in MM cell lines. Our findings provide novel insights into the role of epigenetic gene silencing in MM tumorigenesis and the interplay between the Polycomb repressive complex 2 and DNAme.
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Registered trials
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