ArticleOncogene2018
LSD1 promotes S-phase entry and tumorigenesis via chromatin co-occupation with E2F1 and selective H3K9 demethylation.
Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 49 citations in OpenAlex.
- Dynamic regulation of H3K9 modifications in cancer: pathogenesis and targeted therapies.Biomarker research · 2026Review
- Unraveling the meta-hallmarks between senescent and tumor cells: A new perspective for senolytic drug discovery.Acta pharmaceutica Sinica. B · 2025Review
- KDM1A-driven RNF81 downregulation promotes gastric cancer progression via KLF4 destabilization.Oncogene · 2025Article
- Phase separation of RXRγ drives tumor chemoresistance and represents a therapeutic target for small-cell lung cancer.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Review
- Lysine-specific demethylase 1 (LSD1) suppresses cellular senescence by riboflavin uptake-dependent demethylation activity.Scientific reports · 2025Article
- Dual targeting of KDM1A and antioxidants is an effective anticancer strategy.bioRxiv : the preprint server for biology · 2024Article
- FOXA2 rewires AP-1 for transcriptional reprogramming and lineage plasticity in prostate cancer.Nature communications · 2024Article
- Molecular Mechanisms of Prostate Cancer Development in the Precision Medicine Era: A Comprehensive Review.Cancers · 2024Review
- Repression of LSD1 potentiates homologous recombination-proficient ovarian cancer to PARP inhibitors through down-regulation of BRCA1/2 and RAD51.Nature communications · 2023Article
- Inhibition of LSD1 induces ferroptosis through the ATF4-xCT pathway and shows enhanced anti-tumor effects with ferroptosis inducers in NSCLC.Cell death & disease · 2023Article
- LSD1 promotes prostate cancer reprogramming by repressing TP53 signaling independently of its demethylase function.JCI insight · 2023Article
- Targeting epigenetic regulators to overcome drug resistance in cancers.Signal transduction and targeted therapy · 2023Review
- Lineage plasticity and treatment resistance in prostate cancer: the intersection of genetics, epigenetics, and evolution.Frontiers in endocrinology · 2023Review
- Epigenetic (De)regulation in Prostate Cancer.Cancer treatment and research · 2023Article
- Targeting signaling pathways in prostate cancer: mechanisms and clinical trials.Signal transduction and targeted therapy · 2022Review
- SP2509, a Selective Inhibitor of LSD1, Suppresses Retinoblastoma Growth by Downregulating β-catenin Signaling.Investigative ophthalmology & visual science · 2022Article
- LSD1-mediated stabilization of SEPT6 protein activates the TGF-β1 pathway and regulates non-small-cell lung cancer metastasis.Cancer gene therapy · 2022Article
- RB1 loss in castration-resistant prostate cancer confers vulnerability to LSD1 inhibition.Oncogene · 2022Article
- The Role of Epigenetic Change in Therapy-Induced Neuroendocrine Prostate Cancer Lineage Plasticity.Frontiers in endocrinology · 2022Review
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
Histone H3 lysine-9 (H3K9) methylation is essential for retinoblastoma protein (RB)-mediated heterochromatin formation, epigenetic silencing of S-phase genes and permanent cell cycle arrest or cellular senescence. Besides as an H3K4 demethylase, lysine-specific demethylase-1 (LSD1) has been shown to promote H3K9 demethylation. However, it is unexplored whether LSD1 has a causal role in regulating cell cycle entry and senescence. Here we demonstrate that genetic depletion or pharmacological inhibition of LSD1 triggers G1 arrest and cellular senescence. Genome-wide chromatin immunoprecipitation-sequencing analysis reveals that LSD1 binding sites overlap significantly with those bound by the S-phase gene transcription factor E2F1. Gene ontology analysis demonstrates that a large portion of E2F1 and LSD1 cotargeted genes are involved in cell cycle and proliferation. Further analyses show that depletion of LSD1 increases the level of H3K9me2 and thereby represses expression of the LSD1-E2F1 cotarget genes, but has no effects on H3K4me2 level in those loci. In contrast, knockdown of the H3K4me2 reader PHF8 decreases the H3K4me2 level at the LSD1-E2F1 cotargeted loci, but this effect is rescued by codepletion of LSD1. Furthermore, the enzymatic activity of LSD1 is essential for H3K9me2 demethylation at cell cycle gene loci. Notably, cotreatment of chemotherapeutic agent camptothecin enhanced LSD1 inhibitor-induced senescence and growth inhibition of cancer cells in vitro and in mice. Our data reveal LSD1 as a molecular rheostat selectively regulating H3K9 demethylation at cell cycle gene loci, thereby representing a key player in oncogenesis and a viable target for cancer therapy.
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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.