EBF2 Links KMT2D‐Mediated H3K4me1 to Suppress Pancreatic Cancer Progression via Upregulating KLLN
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.
- Standort
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Deutsche Nationalbibliothek Frankfurt am Main
- Umfang
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Online-Ressource
- Sprache
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Englisch
- Erschienen in
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EBF2 Links KMT2D‐Mediated H3K4me1 to Suppress Pancreatic Cancer Progression via Upregulating KLLN ; day:28 ; month:11 ; year:2023 ; extent:15
Advanced science ; (28.11.2023) (gesamt 15)
- Urheber
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Yao, Bing
Xing, Mengying
Meng, Shixin
Li, Shang
Zhou, Jingwan
Zhang, Ming
Yang, Chen
Qu, Shuang
Jin, Yucui
Yuan, Hongyan
Zen, Ke
Ma, Changyan
- DOI
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10.1002/advs.202302037
- URN
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urn:nbn:de:101:1-2023112914111757073183
- Rechteinformation
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Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Letzte Aktualisierung
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15.08.2025, 07:23 MESZ
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Beteiligte
- Yao, Bing
- Xing, Mengying
- Meng, Shixin
- Li, Shang
- Zhou, Jingwan
- Zhang, Ming
- Yang, Chen
- Qu, Shuang
- Jin, Yucui
- Yuan, Hongyan
- Zen, Ke
- Ma, Changyan
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