ArticleThe EMBO journal2013
DPY30 regulates pathways in cellular senescence through ID protein expression.
Article in The EMBO journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 36 citations in OpenAlex.
- Age-associated miR-30e-3p upregulation drives ovarian follicular granulosa cell senescence by targeting DPY30 in laying hens.Poultry science · 2026Article
- Review
- DPY30 Is an Epigenetic Decoupler Linking Replication Stress to Immunoediting in Pancreatic Cancer.Cancer research · 2026Article
- SETD1A Regulates Glycolysis and Senescence of Nucleus Pulposus Cells via H3K4me3-HELZ2/PPARα-HIF1α Axis to Drive Intervertebral Disc Degeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Plasma proteomics identify novel biomarkers and dynamic patterns of biological aging.Journal of advanced research · 2026Article
- DPY30 knockdown suppresses colorectal carcinoma progression via inducing Raf1/MST2-mediated apoptosis.Heliyon · 2024Article
- CD72, a new immune checkpoint molecule, is a novel prognostic biomarker for kidney renal clear cell carcinoma.European journal of medical research · 2023Article
- Identification and validation of DPY30 as a prognostic biomarker and tumor immune microenvironment infiltration characterization in esophageal cancer.Oncology letters · 2023Article
- DPY30 Promotes Proliferation and Cell Cycle Progression of Colorectal Cancer Cells via Mediating H3K4 Trimethylation.International journal of medical sciences · 2023Article
- Induction of senescence upon loss of the Ash2l core subunit of H3K4 methyltransferase complexes.Nucleic acids research · 2022Article
- Review
- The DPY30-H3K4me3 Axis-Mediated PD-L1 Expression in Melanoma.Journal of inflammation research · 2022Article
- AHNAK controls 53BP1-mediated p53 response by restraining 53BP1 oligomerization and phase separation.Molecular cell · 2021Article
- Id1 expression in kidney endothelial cells protects against diabetes-induced microvascular injury.FEBS open bio · 2020Article
- Specific inhibition of DPY30 activity by ASH2L-derived peptides suppresses blood cancer cell growth.Experimental cell research · 2019Article
- Control of Hematopoietic Stem and Progenitor Cell Function through Epigenetic Regulation of Energy Metabolism and Genome Integrity.Stem cell reports · 2019Article
- DPY30 regulates cervical squamous cell carcinoma by mediating epithelial-mesenchymal transition (EMT).OncoTargets and therapy · 2019Article
- DPY30 is required for the enhanced proliferation, motility and epithelial-mesenchymal transition of epithelial ovarian cancer cells.International journal of molecular medicine · 2018Article
- Differential Proteome Analysis of Human Neuroblastoma Xenograft Primary Tumors and Matched Spontaneous Distant Metastases.Scientific reports · 2018Article
- Hijacking a key chromatin modulator creates epigenetic vulnerability for MYC-driven cancer.The Journal of clinical investigation · 2018Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular senescence is an intrinsic defense mechanism to various cellular stresses: while still metabolically active, senescent cells stop dividing and enter a proliferation arrest. Here, we identify DPY30, a member of all mammalian histone H3K4 histone methyltransferases (HMTases), as a key regulator of the proliferation potential of human primary cells. Following depletion of DPY30, cells show a severe proliferation defect and display a senescent phenotype, including a flattened and enlarged morphology, elevated level of reactive oxygen species (ROS), increased SA-β-galactosidase activity, and formation of senescence-associated heterochromatin foci (SAHFs). While DPY30 depletion leads to a reduced level of H3K4me3-marked active chromatin, we observed a concomitant activation of CDK inhibitors, including p16INK4a, independent of H3K4me3. ChIP experiments show that key regulators of cell-cycle progression, including ID proteins, are under direct control of DPY30. Because ID proteins are negative regulators of the transcription factors ETS1/2, depletion of DPY30 leads to the transcriptional activation of p16INK4a by ETS1/2 and thus to a senescent-like phenotype. Ectoptic re-introduction of ID protein expression can partially rescue the senescence-like phenotype induced by DPY30 depletion. Thus, our data indicate that DPY30 controls proliferation by regulating ID proteins expression, which in turn lead to senescence bypass.
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