ArticleEpigenetics
DNA hypomethylation caused by Lsh deletion promotes erythroleukemia development.
Article in Epigenetics. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 39 citations in OpenAlex.
- Dysregulated HELLS expression alters cellular processes and serves as a potential prognostic marker in acute myeloid leukemia.The Journal of biological chemistry · 2026Article
- Staphylococcus aureus α-hemolysin induces DNA methylation changes in human Th1 cells.Immunologic research · 2025Article
- α-Hemolysin from Staphylococcus aureus Changes the Epigenetic Landscape of Th17 Cells.ImmunoHorizons · 2024Article
- Seminars in cell and development biology on histone variants remodelers of H2A variants associated with heterochromatin.Seminars in cell & developmental biology · 2023Review
- The chromatin remodelling protein LSH/HELLS regulates the amount and distribution of DNA hydroxymethylation in the genome.Epigenetics · 2022Article
- Molecular Landscapes and Models of Acute Erythroleukemia.HemaSphere · 2021Review
- LSH mediates gene repression through macroH2A deposition.Nature communications · 2020Article
- Upregulation of the chromatin remodeler HELLS is mediated by YAP1 in Sonic Hedgehog Medulloblastoma.Scientific reports · 2019Article
- The chromatin remodeling protein Lsh alters nucleosome occupancy at putative enhancers and modulates binding of lineage specific transcription factors.Epigenetics · 2019Article
- Specific or not specific recruitment of DNMTs for DNA methylation, an epigenetic dilemma.Clinical epigenetics · 2018Review
- Lsh/HELLS regulates self-renewal/proliferation of neural stem/progenitor cells.Scientific reports · 2017Article
- The LSH/DDM1 Homolog MUS-30 Is Required for Genome Stability, but Not for DNA Methylation in Neurospora crassa.PLoS genetics · 2016Article
- The ATP binding site of the chromatin remodeling homolog Lsh is required for nucleosome density and de novo DNA methylation at repeat sequences.Nucleic acids research · 2015Article
- Long interspersed element-1 (LINE-1): passenger or driver in human neoplasms?PLoS genetics · 2013Review
- Environmental toxicants, epigenetics, and cancer.Advances in experimental medicine and biology · 2013Review
- The ghosts in the machine: DNA methylation and the mystery of differentiation.Biochimica et biophysica acta · 2012Review
- DNMT3B7, a truncated DNMT3B isoform expressed in human tumors, disrupts embryonic development and accelerates lymphomagenesis.Cancer research · 2010Article
- Derepression of an endogenous long terminal repeat activates the CSF1R proto-oncogene in human lymphoma.Nature medicine · 2010Article
- Promoter methylation in prostate cancer and its application for the early detection of prostate cancer using serum and urine samples.Biomarkers in cancer · 2010Review
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
Abstract
Hematopoietic malignancies are frequently associated with DNA hypomethylation but the molecular mechanisms involved in tumor formation remain poorly understood. Here we report that mice lacking Lsh develop leukemia associated with DNA hypomethylation and oncogene activation. Lsh is a member of the SNF2 chromatin remodeling family and is required for de novo methylation of genomic DNA. Mice that received Lsh deficient hematopoietic progenitors showed severe impairment of hematopoiesis, suggesting that Lsh is necessary for normal hematopoiesis. A subset of mice developed erythroleukemia, a tumor that does not spontaneously occur in mice. Tumor tissues were CpG hypomethylated and showed a modest elevation of the transcription factor PU.1, an oncogene that is crucial for Friend virus induced erythroleukemia. Analysis of Lsh(-/-) hematopoietic progenitors revealed widespread DNA hypomethylation at repetitive sequences and hypomethylation at specific retroviral elements within the PU.1 gene. Wild type cells showed Lsh and Dnmt3b binding at the retroviral elements located within the PU.1 gene. On the other hand, Lsh deficient cells had no detectable Dnmt3b association suggesting that Lsh is necessary for recruitment of Dnmt3b to its target. Furthermore, Lsh(-/-) hematopoietic precursors showed impaired suppression of retroviral elements in the PU.1 gene, an increase of PU.1 transcripts and protein levels. Thus DNA hypomethylation caused by Lsh depletion is linked to transcriptional upregulation of retroviral elements and oncogenes such as PU.1 which in turn may promote the development of erythroleukemia in mice.
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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.