Fan Xuan, Na Liu, Bao-Xi Zhang, Wen-Xiao Wen, Yong-Cai Wang, Hui-Feng Zhang, Xiao-Li Wu
{"title":"High expression and regulatory mechanisms of ANGPT1 and HOXA3 in acute myeloid leukemia.","authors":"Fan Xuan, Na Liu, Bao-Xi Zhang, Wen-Xiao Wen, Yong-Cai Wang, Hui-Feng Zhang, Xiao-Li Wu","doi":"10.1016/j.bulcan.2025.01.014","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>Acute Myeloid Leukemia (AML) is a type of leukemia characterized by the malignant clonal proliferation of hematopoietic stem cells in the bone marrow. This study aims to investigate the role of ANGPT1 and HOXA3 in the leukemia cell line KG-1a.</p><p><strong>Methods: </strong>The expression patterns of ANGPT1 and HOXA3 in AML patients were determined by analyzing the TCGA database and clinical samples. Experiments were conducted using the KG-1a cell line, including flow cytometry and SA-β-Gal staining, to knock down ANGPT1 and HOXA3 and evaluate their functions.</p><p><strong>Results: </strong>ANGPT1 and HOXA3 were found to be highly expressed in AML patients. Knocking down ANGPT1 and HOXA3 promoted apoptosis and senescence in KG-1a cells by inhibiting proliferation-related genes and upregulating apoptosis-related genes. There is a reciprocal regulatory relationship between ANGPT1 and HOXA3, forming a positive feedback loop. Treatment with ATRA downregulated the expression of HOXA3 and induced apoptosis in KG-1a cells, highlighting the importance of HOXA3 as a therapeutic target in AML.</p><p><strong>Conclusion: </strong>ANGPT1 and HOXA3 are highly expressed in AML, and knocking them down can promote apoptosis and senescence in leukemia cells. They exhibit a mutual regulatory relationship, forming a positive feedback loop. These findings contribute to a better understanding of the functional roles and regulatory mechanisms of ANGPT1 and HOXA3, and provide new scientific evidence for the treatment and prognosis improvement of AML patients.</p>","PeriodicalId":93917,"journal":{"name":"Bulletin du cancer","volume":" ","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Bulletin du cancer","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1016/j.bulcan.2025.01.014","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Objective: Acute Myeloid Leukemia (AML) is a type of leukemia characterized by the malignant clonal proliferation of hematopoietic stem cells in the bone marrow. This study aims to investigate the role of ANGPT1 and HOXA3 in the leukemia cell line KG-1a.
Methods: The expression patterns of ANGPT1 and HOXA3 in AML patients were determined by analyzing the TCGA database and clinical samples. Experiments were conducted using the KG-1a cell line, including flow cytometry and SA-β-Gal staining, to knock down ANGPT1 and HOXA3 and evaluate their functions.
Results: ANGPT1 and HOXA3 were found to be highly expressed in AML patients. Knocking down ANGPT1 and HOXA3 promoted apoptosis and senescence in KG-1a cells by inhibiting proliferation-related genes and upregulating apoptosis-related genes. There is a reciprocal regulatory relationship between ANGPT1 and HOXA3, forming a positive feedback loop. Treatment with ATRA downregulated the expression of HOXA3 and induced apoptosis in KG-1a cells, highlighting the importance of HOXA3 as a therapeutic target in AML.
Conclusion: ANGPT1 and HOXA3 are highly expressed in AML, and knocking them down can promote apoptosis and senescence in leukemia cells. They exhibit a mutual regulatory relationship, forming a positive feedback loop. These findings contribute to a better understanding of the functional roles and regulatory mechanisms of ANGPT1 and HOXA3, and provide new scientific evidence for the treatment and prognosis improvement of AML patients.