{"title":"错误表达的FOXC1对RUNX1、HDAC1和TLE3共阻遏物复合物的增强子募集阻断急性髓系白血病的分化","authors":"Fabrizio Simeoni, Tim Cp Somervaille","doi":"10.1080/23723556.2021.2003161","DOIUrl":null,"url":null,"abstract":"<p><p>Tissue-inappropriate expression of <i>FOXC1</i> (Forkhead Box C1) in acute myeloid leukemia confers a monocyte/macrophage lineage differentiation block. We discovered that FOXC1 interacts with RUNX1 (Runt-Related Transcription Factor 1) to stabilize a RUNX1, HDAC1 (Histone Deacetylase 1) and TLE3 (Transducin-like enhancer protein 3) repressor complex at enhancers controlling myeloid differentiation genes.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":null,"pages":null},"PeriodicalIF":2.6000,"publicationDate":"2021-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8997249/pdf/","citationCount":"0","resultStr":"{\"title\":\"Enhancer recruitment of a RUNX1, HDAC1 and TLE3 co-repressor complex by mis-expressed FOXC1 blocks differentiation in acute myeloid leukemia.\",\"authors\":\"Fabrizio Simeoni, Tim Cp Somervaille\",\"doi\":\"10.1080/23723556.2021.2003161\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Tissue-inappropriate expression of <i>FOXC1</i> (Forkhead Box C1) in acute myeloid leukemia confers a monocyte/macrophage lineage differentiation block. We discovered that FOXC1 interacts with RUNX1 (Runt-Related Transcription Factor 1) to stabilize a RUNX1, HDAC1 (Histone Deacetylase 1) and TLE3 (Transducin-like enhancer protein 3) repressor complex at enhancers controlling myeloid differentiation genes.</p>\",\"PeriodicalId\":37292,\"journal\":{\"name\":\"Molecular and Cellular Oncology\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":2.6000,\"publicationDate\":\"2021-11-19\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8997249/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Molecular and Cellular Oncology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1080/23723556.2021.2003161\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2021/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q3\",\"JCRName\":\"ONCOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Molecular and Cellular Oncology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1080/23723556.2021.2003161","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2021/1/1 0:00:00","PubModel":"eCollection","JCR":"Q3","JCRName":"ONCOLOGY","Score":null,"Total":0}
Enhancer recruitment of a RUNX1, HDAC1 and TLE3 co-repressor complex by mis-expressed FOXC1 blocks differentiation in acute myeloid leukemia.
Tissue-inappropriate expression of FOXC1 (Forkhead Box C1) in acute myeloid leukemia confers a monocyte/macrophage lineage differentiation block. We discovered that FOXC1 interacts with RUNX1 (Runt-Related Transcription Factor 1) to stabilize a RUNX1, HDAC1 (Histone Deacetylase 1) and TLE3 (Transducin-like enhancer protein 3) repressor complex at enhancers controlling myeloid differentiation genes.
期刊介绍:
For a long time, solid neoplasms have been viewed as relatively homogeneous entities composed for the most part of malignant cells. It is now clear that tumors are highly heterogeneous structures that evolve in the context of intimate interactions between cancer cells and endothelial, stromal as well as immune cells. During the past few years, experimental and clinical oncologists have witnessed several conceptual transitions of this type. Molecular and Cellular Oncology (MCO) emerges within this conceptual framework as a high-profile forum for the publication of fundamental, translational and clinical research on cancer. The scope of MCO is broad. Submissions dealing with all aspects of oncogenesis, tumor progression and response to therapy will be welcome, irrespective of whether they focus on solid or hematological neoplasms. MCO has gathered leading scientists with expertise in multiple areas of cancer research and other fields of investigation to constitute a large, interdisciplinary, Editorial Board that will ensure the quality of articles accepted for publication. MCO will publish Original Research Articles, Brief Reports, Reviews, Short Reviews, Commentaries, Author Views (auto-commentaries) and Meeting Reports dealing with all aspects of cancer research.