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http://purl.uniprot.org/citations/37157016http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/37157016http://www.w3.org/2000/01/rdf-schema#comment"Internal tandem duplication (ITD) mutations within the FMS-like tyrosine kinase-3 (FLT3) occur in up to 25% of acute myeloid leukemia (AML) patients and indicate a very poor prognosis. The role of long noncoding RNAs (lncRNAs) in FLT3-ITD AML progression remains unexplored. We identified a novel lncRNA, SNHG29, whose expression is specifically regulated by the FLT3-STAT5 signaling pathway and is abnormally down-regulated in FLT3-ITD AML cell lines. SNHG29 functions as a tumor suppressor, significantly inhibiting FLT3-ITD AML cell proliferation and decreasing sensitivity to cytarabine in vitro and in vivo models. Mechanistically, we demonstrated that SNHG29's molecular mechanism is EP300-binding dependent and identified the EP300-interacting region of SNHG29. SNHG29 modulates genome-wide EP300 genomic binding, affecting EP300-mediated histone modification and consequently influencing the expression of varies downstream AML-associated genes. Our study uncovers a novel molecular mechanism for SNHG29 in mediating FLT3-ITD AML biological behaviors through epigenetic modification, suggesting that SNHG29 could be a potential therapeutic target for FLT3-ITD AML."xsd:string
http://purl.uniprot.org/citations/37157016http://purl.org/dc/terms/identifier"doi:10.1038/s41375-023-01923-y"xsd:string
http://purl.uniprot.org/citations/37157016http://purl.uniprot.org/core/author"Chen Z."xsd:string
http://purl.uniprot.org/citations/37157016http://purl.uniprot.org/core/author"Chen W."xsd:string
http://purl.uniprot.org/citations/37157016http://purl.uniprot.org/core/author"Chen B."xsd:string
http://purl.uniprot.org/citations/37157016http://purl.uniprot.org/core/author"Chen D."xsd:string
http://purl.uniprot.org/citations/37157016http://purl.uniprot.org/core/author"Liu S."xsd:string
http://purl.uniprot.org/citations/37157016http://purl.uniprot.org/core/author"Lin Y."xsd:string
http://purl.uniprot.org/citations/37157016http://purl.uniprot.org/core/author"Zhou J."xsd:string
http://purl.uniprot.org/citations/37157016http://purl.uniprot.org/core/author"Shang J."xsd:string
http://purl.uniprot.org/citations/37157016http://purl.uniprot.org/core/author"Ye X."xsd:string
http://purl.uniprot.org/citations/37157016http://purl.uniprot.org/core/date"2023"xsd:gYear
http://purl.uniprot.org/citations/37157016http://purl.uniprot.org/core/name"Leukemia"xsd:string
http://purl.uniprot.org/citations/37157016http://purl.uniprot.org/core/pages"1421-1434"xsd:string
http://purl.uniprot.org/citations/37157016http://purl.uniprot.org/core/title"A novel lncRNA SNHG29 regulates EP300- related histone acetylation modification and inhibits FLT3-ITD AML development."xsd:string
http://purl.uniprot.org/citations/37157016http://purl.uniprot.org/core/volume"37"xsd:string
http://purl.uniprot.org/citations/37157016http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/37157016
http://purl.uniprot.org/citations/37157016http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/37157016
http://purl.uniprot.org/uniprot/#_Q8WUR1-mappedCitation-37157016http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/37157016
http://purl.uniprot.org/uniprot/#_Q7Z306-mappedCitation-37157016http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/37157016
http://purl.uniprot.org/uniprot/#_Q96EF2-mappedCitation-37157016http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/37157016
http://purl.uniprot.org/uniprot/Q8WUR1http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/37157016
http://purl.uniprot.org/uniprot/Q96EF2http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/37157016
http://purl.uniprot.org/uniprot/Q7Z306http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/37157016