ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024
EBF2 Links KMT2D-Mediated H3K4me1 to Suppress Pancreatic Cancer Progression via Upregulating KLLN.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Targeting CCR7-KMT2D enhances CAR-T cell efficacy by suppressing therapy-induced senescence in B-cell non-Hodgkin lymphoma.BMC medicine · 2026Article
- EBF3 suppresses lung adenocarcinoma progression and immune evasion via transcriptional repression of CCL24.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- YTH Domain Family 2 Promotes Tubal Factor Infertility through Reducing H3K4me1 Methylation of CYLD by KMT2D.Applied biochemistry and biotechnology · 2026Article
- Development of Dimethylsulfonium Probes for Broad Profiling of Methyllysine Reader Proteins.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Postnatal expression of the transcription factor Ebf2 in motivation, reward, and pain-related circuits of the mouse brain.Frontiers in neuroanatomy · 2026Article
- SETD7-mediated H3K4me1 activates ALDH1A3 to drive ferroptosis resistance in esophageal squamous cell carcinoma.Cell death & disease · 2025Article
- Insights into the mechanisms driven by H3K4 KMTs in pancreatic cancer.The Biochemical journal · 2024Review
- EBF2 Links KMT2D-Mediated H3K4me1 to Suppress Pancreatic Cancer Progression via Upregulating KLLN.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Mono-methylation of histone H3 on Lys 4 (H3K4me1), which is catalyzed by histone-lysine N-methyltransferase 2D (KMT2D), serves as an important epigenetic regulator in transcriptional control. In this study, the authors identify early B-cell factor 2 (EBF2) as a binding protein of H3K4me1. Combining analyses of RNA-seq and ChIP-seq data, the authors further identify killin (KLLN) as a transcriptional target of KMT2D and EBF2 in pancreatic ductal adenocarcinoma (PDAC) cells. KMT2D-dependent H3K4me1 and EBF2 are predominantly over-lapped proximal to the transcription start site (TSS) of KLLN gene. Comprehensive functional assays show that KMT2D and EBF2 cooperatively inhibit PDAC cells proliferation, migration, and invasion through upregulating KLLN. Such inhibition on PDAC progression is also achieved through increasing H3K4me1 level by GSK-LSD1, a selective inhibitor of lysine-specific demethylase 1 (LSD1). Taken together, these findings reveal a new mechanism underlying PDAC progression and provide potential therapeutic targets for PDAC treatment.
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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.