ArticleNucleic acids research2018
Combined cistrome and transcriptome analysis of SKI in AML cells identifies SKI as a co-repressor for RUNX1.
Article in Nucleic acids research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- The Diagnostic Potential and Regulatory Mechanisms of miR-3180-3p in Metabolic Dysfunction-Associated Fatty Liver Disease with Respect to Inflammation and Oxidative Stress.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2025Article
- JMJD1C forms condensate to facilitate a RUNX1-dependent gene expression program shared by multiple types of AML cells.Protein & cell · 2025Article
- c-Ski is a novel repressor of NF-κB through interaction with p65 and HDAC1 in U937 cells.Cell communication and signaling : CCS · 2025Article
- Differential regulation of Treg stability in human naïve and effector Treg subsets by TGFβ-signaling via ARKADIA-SKI axis.Frontiers in immunology · 2025Article
- Identification of a novelFrontiers in oncology · 2025Article
- Ski ameliorates synovial cell inflammation in monosodium iodoacetate-induced knee osteoarthritis.Heliyon · 2024Article
- Pre-configuring chromatin architecture with histone modifications guides hematopoietic stem cell formation in mouse embryos.Nature communications · 2022Article
- The Oncoprotein SKI Acts as A Suppressor of NK Cell-Mediated Immunosurveillance in PDAC.Cancers · 2020Article
- Nuclear interacting SET domain protein 1 inactivation impairs GATA1-regulated erythroid differentiation and causes erythroleukemia.Nature communications · 2020Article
- Single-cell multiomic analysis identifies regulatory programs in mixed-phenotype acute leukemia.Nature biotechnology · 2019Article
- Genomics-Guided Immunotherapy for Precision Medicine in Cancer.Cancer biotherapy & radiopharmaceuticals · 2019Review
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
SKI is a transcriptional co-regulator and overexpressed in various human tumors, for example in acute myeloid leukemia (AML). SKI contributes to the origin and maintenance of the leukemic phenotype. Here, we use ChIP-seq and RNA-seq analysis to identify the epigenetic alterations induced by SKI overexpression in AML cells. We show that approximately two thirds of differentially expressed genes are up-regulated upon SKI deletion, of which >40% harbor SKI binding sites in their proximity, primarily in enhancer regions. Gene ontology analysis reveals that many of the differentially expressed genes are annotated to hematopoietic cell differentiation and inflammatory response, corroborating our finding that SKI contributes to a myeloid differentiation block in HL60 cells. We find that SKI peaks are enriched for RUNX1 consensus motifs, particularly in up-regulated SKI targets upon SKI deletion. RUNX1 ChIP-seq displays that nearly 70% of RUNX1 binding sites overlap with SKI peaks, mainly at enhancer regions. SKI and RUNX1 occupy the same genomic sites and cooperate in gene silencing. Our work demonstrates for the first time the predominant co-repressive function of SKI in AML cells on a genome-wide scale and uncovers the transcription factor RUNX1 as an important mediator of SKI-dependent transcriptional repression.
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