ArticlePloS one2012
Genome-wide characterization of menin-dependent H3K4me3 reveals a specific role for menin in the regulation of genes implicated in MEN1-like tumors.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 56 citations in OpenAlex.
- Review
- Menin: from molecular insights to clinical impact.Epigenomics · 2025Review
- Homologous recombination deficiency in pancreatic neuroendocrine tumors.Future oncology (London, England) · 2024Article
- Menin in Cancer.Genes · 2024Review
- Pancreatic Neuroendocrine Tumors: Signaling Pathways and Epigenetic Regulation.International journal of molecular sciences · 2024Review
- A Molecular Switch between Mammalian MLL Complexes Dictates Response to Menin-MLL Inhibition.Cancer discovery · 2023Article
- Risk Stratification of Pancreatic Neuroendocrine Neoplasms Based on Clinical, Pathological, and Molecular Characteristics.Journal of clinical medicine · 2022Review
- Mice With RIP-Cre-mediated Deletion of the Long Noncoding RNAJournal of the Endocrine Society · 2022Article
- Modeling MEN1 with Patient-Origin iPSCs Reveals GLP-1R Mediated Hypersecretion of Insulin.Cells · 2022Article
- Dichotomous Roles ofInternational journal of molecular sciences · 2022Article
- Menin directs regionalized decidual transformation through epigenetically setting PTX3 to balance FGF and BMP signaling.Nature communications · 2022Article
- Molecular biology of pancreatic neuroendocrine tumors: From mechanism to translation.Frontiers in oncology · 2022Review
- Review
- Review
- H3K4 Methylation in Aging and Metabolism.Epigenomes · 2021Review
- Multiple Endocrine Neoplasia Type 1: Latest Insights.Endocrine reviews · 2021Review
- Epigenetic regulation in the tumorigenesis of MEN1-associated endocrine cell types.Journal of molecular endocrinology · 2018Review
- Long Noncoding RNA MEG3 Is an Epigenetic Determinant of Oncogenic Signaling in Functional Pancreatic Neuroendocrine Tumor Cells.Molecular and cellular biology · 2017Article
- Twenty years of menin: emerging opportunities for restoration of transcriptional regulation in MEN1.Endocrine-related cancer · 2017Review
- The future: genetics advances in MEN1 therapeutic approaches and management strategies.Endocrine-related cancer · 2017Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Inactivating mutations in the MEN1 gene predisposing to the multiple endocrine neoplasia type 1 (MEN1) syndrome can also cause sporadic pancreatic endocrine tumors. MEN1 encodes menin, a subunit of MLL1/MLL2-containing histone methyltransferase complexes that trimethylate histone H3 at lysine 4 (H3K4me3). The importance of menin-dependent H3K4me3 in normal and transformed pancreatic endocrine cells is unclear. To study the role of menin-dependent H3K4me3, we performed in vitro differentiation of wild-type as well as menin-null mouse embryonic stem cells (mESCs) into pancreatic islet-like endocrine cells (PILECs). Gene expression analysis and genome-wide H3K4me3 ChIP-Seq profiling in wild-type and menin-null mESCs and PILECs revealed menin-dependent H3K4me3 at the imprinted Dlk1-Meg3 locus in mESCs, and all four Hox loci in differentiated PILECs. Specific and significant loss of H3K4me3 and gene expression was observed for genes within the imprinted Dlk1-Meg3 locus in menin-null mESCs and the Hox loci in menin-null PILECs. Given that the reduced expression of genes within the DLK1-MEG3 locus and the HOX loci is associated with MEN1-like sporadic tumors, our data suggests a possible role for menin-dependent H3K4me3 at these genes in the initiation and progression of sporadic pancreatic endocrine tumors. Furthermore, our investigation also demonstrates that menin-null mESCs can be differentiated in vitro into islet-like endocrine cells, underscoring the utility of menin-null mESC-derived specialized cell types for genome-wide high-throughput studies.
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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.