ArticleCell death & disease2019
SETD3 is a positive regulator of DNA-damage-induced apoptosis.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.
- Molecular Biomarkers of Radiosensitivity and Radioresistance in Cervical Cancer: A Systematic Review.International journal of molecular sciences · 2026Pooled it
- Functional Analysis of the Histidine N-Methyltransferase SETD3 in Endometriosis.International journal of molecular sciences · 2026Article
- The emerging paradigms of SETD family enzymes as epigenetic regulators of the immune response in inflammatory diseases.Frontiers in immunology · 2026Review
- SETD3 regulates Bcl-6 expression and Tfh differentiation in SLE CD4Clinical epigenetics · 2025Article
- Article
- The methyltransferase SETD3 regulates mRNA alternative splicing through interacting with hnRNPK.Cell insight · 2024Article
- Cell fate regulation governed by p53: Friends or reversible foes in cancer therapy.Cancer communications (London, England) · 2024Review
- Tumor-suppressive functions of protein lysine methyltransferases.Experimental & molecular medicine · 2023Review
- SETD4-mediated KU70 methylation suppresses apoptosis.Cell reports · 2022Article
- Stabilization of SETD3 by deubiquitinase USP27 enhances cell proliferation and hepatocellular carcinoma progression.Cellular and molecular life sciences : CMLS · 2022Article
- SETD3 Methyltransferase Regulates PLK1 Expression to PromoteFrontiers in oncology · 2022Article
- Reduction of H3K27cr Modification During DNA Damage in Colon Cancer.Frontiers in oncology · 2022Article
- p53 signaling in cancer progression and therapy.Cancer cell international · 2021Review
- Article
- The Structure, Activity, and Function of the SETD3 Protein Histidine Methyltransferase.Life (Basel, Switzerland) · 2021Review
- SETD3 Downregulation Mediates PTEN Upregulation-Induced Ischemic Neuronal Death Through Suppression of Actin Polymerization and Mitochondrial Function.Molecular neurobiology · 2021Article
- Transcriptional regulation by methyltransferases and their role in the heart: highlighting novel emerging functionality.American journal of physiology. Heart and circulatory physiology · 2020Review
- circSETD3 Contributes to Acquired Resistance to Gefitinib in Non-Small-Cell Lung Cancer by Targeting the miR-520h/ABCG2 Pathway.Molecular therapy. Nucleic acids · 2020Article
- Deletion of Mouse Setd4 Promotes the Recovery of Hematopoietic Failure.International journal of radiation oncology, biology, physics · 2020Article
- Regulating tumor suppressor genes: post-translational modifications.Signal transduction and targeted therapy · 2020Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
SETD3 is a member of the protein lysine methyltransferase (PKMT) family, which catalyzes the addition of methyl group to lysine residues. However, the protein network and the signaling pathways in which SETD3 is involved remain largely unexplored. In the current study, we show that SETD3 is a positive regulator of DNA-damage-induced apoptosis in colon cancer cells. Our data indicate that depletion of SETD3 from HCT-116 cells results in a significant inhibition of apoptosis after doxorubicin treatment. Our results imply that the positive regulation is sustained by methylation, though the substrate remains unknown. We present a functional cross-talk between SETD3 and the tumor suppressor p53. SETD3 binds p53 in cells in response to doxorubicin treatment and positively regulates p53 target genes activation under these conditions. Mechanistically, we provide evidence that the presence of SETD3 and its catalytic activity is required for the recruitment of p53 to its target genes. Finally, Kaplan-Meier survival analysis, of two-independent cohorts of colon cancer patients, revealed that low expression of SETD3 is a reliable predictor of poor survival in these patients, which correlates with our findings. Together, our data uncover a new role of the PKMT SETD3 in the regulation of p53-dependent activation of apoptosis in response to DNA damage.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.