Jinhuan Xu, Xi Ming, Jiaying Wu, Wanying Liu, Yi Xiao
{"title":"Circ_0035381 contributes to the progression of acute myeloid leukemia via regulating miR-186-5p/CDCA3 pathway.","authors":"Jinhuan Xu, Xi Ming, Jiaying Wu, Wanying Liu, Yi Xiao","doi":"10.1080/17474086.2025.2484377","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Circular RNAs (circRNAs) are involved in acute myeloid leukemia (AML) and may be useful for AML therapy. Herein, the project aimed to explore the functions and mechanisms of circ_0035381 in AML.</p><p><strong>Research design and methods: </strong>Circ_0035381, microRNA-186-5p (miR-186-5p), and cell division cycle associated 3 (CDCA3) expression were determined using quantitative real-time polymerase chain reaction (qRT-PCR) assay. Western blot assay was used to measure protein levels. 5'-ethynyl-2'-deoxyuridine (EdU) and flow cytometry were adopted to measure cell proliferation and apoptosis. Glucose consumption and lactate uptake were examined with commercial kits. The relationships between miR-186-5p and circ_0035381 or CDCA3 were validated using dual-luciferase reporter and RNA pull-down assays.</p><p><strong>Results: </strong>Circ_0035381 was increased in the AML subject and AML cell line. Circ_0035381 deficiency hindered the proliferation and glycolysis level and promoted apoptosis in the AML cell line. Circ_0035381 sponged miR-186-5p and miR-186-5p inhibition reversed the effect of circ_0035381 knockdown on AML cell progression. CDCA3 was the target gene of miR-186-5p. CDCA3 overexpression reversed circ_0035381 knockdown-mediated AML cell proliferation and glycolysis inhibition and apoptosis promotion.</p><p><strong>Conclusions: </strong>Circ_0035381 promoted AML progression by elevating CDCA3 through sponging miR-186-5p, providing some clues for the diagnosis and treatment of AML.</p>","PeriodicalId":12325,"journal":{"name":"Expert Review of Hematology","volume":" ","pages":"425-434"},"PeriodicalIF":2.1000,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Expert Review of Hematology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/17474086.2025.2484377","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/4/22 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"HEMATOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Background: Circular RNAs (circRNAs) are involved in acute myeloid leukemia (AML) and may be useful for AML therapy. Herein, the project aimed to explore the functions and mechanisms of circ_0035381 in AML.
Research design and methods: Circ_0035381, microRNA-186-5p (miR-186-5p), and cell division cycle associated 3 (CDCA3) expression were determined using quantitative real-time polymerase chain reaction (qRT-PCR) assay. Western blot assay was used to measure protein levels. 5'-ethynyl-2'-deoxyuridine (EdU) and flow cytometry were adopted to measure cell proliferation and apoptosis. Glucose consumption and lactate uptake were examined with commercial kits. The relationships between miR-186-5p and circ_0035381 or CDCA3 were validated using dual-luciferase reporter and RNA pull-down assays.
Results: Circ_0035381 was increased in the AML subject and AML cell line. Circ_0035381 deficiency hindered the proliferation and glycolysis level and promoted apoptosis in the AML cell line. Circ_0035381 sponged miR-186-5p and miR-186-5p inhibition reversed the effect of circ_0035381 knockdown on AML cell progression. CDCA3 was the target gene of miR-186-5p. CDCA3 overexpression reversed circ_0035381 knockdown-mediated AML cell proliferation and glycolysis inhibition and apoptosis promotion.
Conclusions: Circ_0035381 promoted AML progression by elevating CDCA3 through sponging miR-186-5p, providing some clues for the diagnosis and treatment of AML.
期刊介绍:
Advanced molecular research techniques have transformed hematology in recent years. With improved understanding of hematologic diseases, we now have the opportunity to research and evaluate new biological therapies, new drugs and drug combinations, new treatment schedules and novel approaches including stem cell transplantation. We can also expect proteomics, molecular genetics and biomarker research to facilitate new diagnostic approaches and the identification of appropriate therapies. Further advances in our knowledge regarding the formation and function of blood cells and blood-forming tissues should ensue, and it will be a major challenge for hematologists to adopt these new paradigms and develop integrated strategies to define the best possible patient care. Expert Review of Hematology (1747-4086) puts these advances in context and explores how they will translate directly into clinical practice.