ArticleNature communications2019
SETD1A protects from senescence through regulation of the mitotic gene expression program.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
42 citing papers in PubMed, 87 citations in OpenAlex.
- High-throughput proteomics of breast cancer interstitial fluid: identification of tumor subtype-specific serologically relevant biomarkers.Molecular oncology · 2021Trial
- Clinical, cellular, and genomic consequences of a population-enrichedResearch square · 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
- Set1 promotes Notch-induced transcriptional activation.Cellular and molecular life sciences : CMLS · 2026Article
- Integrated epigenetic networks in aging: from histone to RNA modifications.Journal of translational medicine · 2026Review
- Setd1a Loss-of-function Disrupts Epigenetic Regulation of Ribosomal Genes via Altered DNA Methylation.Schizophrenia bulletin · 2026Article
- Heritable changes in chromatin contacts associated with transgenerational susceptibility to diet-induced insulin dysregulation and obesity.Nature communications · 2026Article
- FOXA2 as a SETD1A-Regulated Driver of Tamoxifen Resistance in Breast Cancer.Oncology research · 2026Article
- HORMAD1 inhibits senescence and promotes proliferation of triple negative breast cancer by facilitating ubiquitination-mediated degradation of p27.American journal of translational research · 2026Article
- Canonical and Non-Canonical Functions of Histone H3K4 Methylation Modifiers in Cancer.Cancer science · 2025Review
- Non-catalytic role of SETD1A promotes gastric cancer cell proliferation through the E2F4-TAF6 axis in the cell cycle.Cell death & disease · 2025Article
- Non-enzymatic SETD1A activity drives breast cancer cell proliferation via cyclin K.Breast cancer research : BCR · 2025Article
- Gene age gap estimate (GAGE) for major depressive disorder: A penalized biological age model using gene expression.Neurobiology of aging · 2025Article
- Novel Approach to Overcome Osimertinib Resistance Using Bromodomain and Extra-Terminal Domain Inhibitors.Cancer science · 2025Article
- Exploring the potential anti-senescence effects of soybean-derived peptide Soymetide in mice hippocampal neurons via the Wnt/β-catenin pathway.Frontiers in pharmacology · 2025Article
- Challenges in the Development of Novel Therapies for Thoracic Malignancies.Juntendo medical journal · 2025Review
- Epigenetic Modifiers: Exploring the Roles of Histone Methyltransferases and Demethylases in Cancer and Neurodegeneration.Biology · 2024Review
- Graph Fourier transform for spatial omics representation and analyses of complex organs.Nature communications · 2024Article
- The COMPASS complex maintains the metastatic capacity imparted by a subpopulation of cells in UPS.iScience · 2024Article
- KMT2 Family of H3K4 Methyltransferases: Enzymatic Activity-dependent and -independent Functions.Journal of molecular biology · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 2 institutions in 2 countries.
Funding
Abstract
SETD1A, a Set1/COMPASS family member maintaining histone-H3-lysine-4 (H3K4) methylation on transcriptionally active promoters, is overexpressed in breast cancer. Here, we show that SETD1A supports mitotic processes and consequentially, its knockdown induces senescence. SETD1A, through promoter H3K4 methylation, regulates several genes orchestrating mitosis and DNA-damage responses, and its depletion causes chromosome misalignment and segregation defects. Cell cycle arrest in SETD1A knockdown senescent cells is independent of mutations in p53, RB and p16, known senescence mediators; instead, it is sustained through transcriptional suppression of SKP2, which degrades p27 and p21. Rare cells escaping senescence by restoring SKP2 expression display genomic instability. In > 200 cancer cell lines and in primary circulating tumor cells, SETD1A expression correlates with genes promoting mitosis and cell cycle suggesting a broad role in suppressing senescence induced by aberrant mitosis. Thus, SETD1A is essential to maintain mitosis and proliferation and its suppression unleashes the tumor suppressive effects of senescence.
Indexed as
Identifiers
What OpenQuestion holds
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.