{"database":"biostudies-literature","file_versions":[],"scores":{"citationCount":0,"reanalysisCount":0,"viewCount":49,"searchCount":0},"additional":{"omics_type":["Unknown"],"volume":["11"],"submitter":["Zhang W"],"pubmed_abstract":["Acute myeloid leukemia (AML) is an aggressive hematological malignancy with high relapse/refractory rate. Genetic and epigenetic abnormalities are driving factors for leukemogenesis. RUNX1 and RUNX2 from the Runt-related transcription factor (RUNX) family played important roles in AML pathogenesis. However, the relationship between RUNX3 and AML remains unclear. Here, we found that <i>RUNX3</i> was a super-enhancer-associated gene and highly expressed in AML cells. The Cancer Genome Atlas (TCGA) database showed high expression of <i>RUNX3</i> correlated with poor prognosis of AML patients. We observed that <i>Runx3</i> knockdown significantly inhibited leukemia progression by inducing DNA damage to enhance apoptosis in murine AML cells. By chromatin immunoprecipitation sequencing (ChIP-seq) analysis, we discovered that RUNX3 in AML cells mainly bound more genes involved in DNA-damage repair and antiapoptosis pathways compared to that in normal bone marrow cells. <i>Runx3</i> knockdown obviously inhibited the expression of these genes in AML cells. Overall, we identified <i>RUNX3</i> as an oncogene overexpressed in AML cells, and <i>Runx3</i> knockdown suppressed AML progression by inducing DNA damage and apoptosis."],"journal":["Frontiers in oncology"],"pagination":["725336"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8549545"],"repository":["biostudies-literature"],"pubmed_title":["Runt-Related Transcription Factor 3 Promotes Acute Myeloid Leukemia Progression."],"pmcid":["PMC8549545"],"pubmed_authors":["Zhang W","Ma Q","Zhao M","Liu L","Lin D","Long B","Sun Z"],"view_count":["49"],"additional_accession":[]},"is_claimable":false,"name":"Runt-Related Transcription Factor 3 Promotes Acute Myeloid Leukemia Progression.","description":"Acute myeloid leukemia (AML) is an aggressive hematological malignancy with high relapse/refractory rate. Genetic and epigenetic abnormalities are driving factors for leukemogenesis. RUNX1 and RUNX2 from the Runt-related transcription factor (RUNX) family played important roles in AML pathogenesis. However, the relationship between RUNX3 and AML remains unclear. Here, we found that <i>RUNX3</i> was a super-enhancer-associated gene and highly expressed in AML cells. The Cancer Genome Atlas (TCGA) database showed high expression of <i>RUNX3</i> correlated with poor prognosis of AML patients. We observed that <i>Runx3</i> knockdown significantly inhibited leukemia progression by inducing DNA damage to enhance apoptosis in murine AML cells. By chromatin immunoprecipitation sequencing (ChIP-seq) analysis, we discovered that RUNX3 in AML cells mainly bound more genes involved in DNA-damage repair and antiapoptosis pathways compared to that in normal bone marrow cells. <i>Runx3</i> knockdown obviously inhibited the expression of these genes in AML cells. Overall, we identified <i>RUNX3</i> as an oncogene overexpressed in AML cells, and <i>Runx3</i> knockdown suppressed AML progression by inducing DNA damage and apoptosis.","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021","modification":"2024-11-13T03:19:01.704Z","creation":"2022-02-11T12:25:58.936Z"},"accession":"S-EPMC8549545","cross_references":{"pubmed":["34722267"],"doi":["10.3389/fonc.2021.725336"]}}