Blood: Increased CTCF occupancy in AML cells is associated with its abnormal expression genes

CTCF is the key regulatory factor for gene expression, and CTCF plays a role through tissue chromatin structureIt is not clear how CTCF combinations are disturbed in leukemia or general cancerMujahed et alstudied CTCF binding in cells and normal bone marrow (NBM) in patients with acute myeloid leukemia (AML) through ChIP-Seq in the context of gene expression, DNA methylation, and exposure to nitrogen synchrocantshas more CTCF combinations in AML than NBMCTCF combines anomalies on key myelin transcription factor molds such as CEBPA, PU.1, and RUNX1AML carrying the TET2 mutation is characterized by a particularly strong combination force of CTCF, which is highly rich in the initiation subregion, but is usually enriched in the enhanced sub-region in the general AMLThere is a strong countercorrelation between CTCF binding and DNA methylationThe increase in CTCF occupation is associated with an increase in gene expression, but the enrichment of genomic location (promoter vs far-end region) and base sequence (inhibition cofactor vs activation cofactor) play a decisive role in gene expression patternsknockout of CTCF in K562 cells leads to loss of CTCF binding and transcription inhibition of genes that alter CTCF binding in AML, as well as the loss of RUNX1/CTCF binding at the RUNX1/CTCF binding siteIn addition, knocking down CTCF can lead to increased differentiationnitrogen synchtoside exposure led to a significant change in CTCF occupancy of cells in AML patients, and some CTCF binding patterns reverted to a Similar TonBMin general, this study suggests an unusual increase in CTCF occupancy rates in AML, targeting genes critical to the development of AML and their expression