Circ_0035381通过调控miR-186-5p/CDCA3通路参与急性髓系白血病的进展。

IF 2.1 4区 医学 Q2 HEMATOLOGY
Expert Review of Hematology Pub Date : 2025-04-01 Epub Date: 2025-04-22 DOI:10.1080/17474086.2025.2484377
Jinhuan Xu, Xi Ming, Jiaying Wu, Wanying Liu, Yi Xiao
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引用次数: 0

摘要

背景:环状rna (circRNAs)参与急性髓性白血病(AML),可能对AML治疗有用。本课题旨在探讨circ_0035381在AML中的作用及机制。研究设计和方法:采用实时定量聚合酶链反应(qRT-PCR)法检测Circ_0035381、microRNA-186-5p (miR-186-5p)和细胞分裂周期相关3 (CDCA3)的表达。Western blot法检测蛋白水平。采用5′-乙基-2′-脱氧尿苷(EdU)和流式细胞术检测细胞增殖和凋亡。用商用试剂盒检测葡萄糖消耗和乳酸摄取。通过双荧光素酶报告基因和RNA下拉试验验证miR-186-5p与circ_0035381或CDCA3之间的关系。结果:Circ_0035381在AML受试者和AML细胞系中表达升高。Circ_0035381缺乏抑制AML细胞增殖和糖酵解水平,促进细胞凋亡。Circ_0035381海绵miR-186-5p和miR-186-5p抑制逆转了Circ_0035381敲除对AML细胞进展的影响。CDCA3是miR-186-5p的靶基因。CDCA3过表达逆转circ_0035381敲低介导的AML细胞增殖、糖酵解抑制和细胞凋亡促进。结论:Circ_0035381通过海绵miR-186-5p上调CDCA3促进AML进展,为AML的诊断和治疗提供一定线索。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Circ_0035381 contributes to the progression of acute myeloid leukemia via regulating miR-186-5p/CDCA3 pathway.

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.

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来源期刊
CiteScore
4.70
自引率
3.60%
发文量
98
审稿时长
6-12 weeks
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.
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