{"title":"[DYRK1A在急性髓系白血病阿糖胞苷耐药中的作用机制]。","authors":"Jia-Wei Feng, Hong-Juan Yu","doi":"10.19746/j.cnki.issn.1009-2137.2025.03.004","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>To investigate the role of <i>DYRK1A</i> in the cytarabine (Ara-C) resistance mechanism of acute myeloid leukemia (AML) cells.</p><p><strong>Methods: </strong>Overexpression and silencing of <i>DYRK1A</i> gene in THP-1 cells were used to observe whether the sensitivity of THP-1 cells to Ara-C was altered. RT-PCR was used to detect the changes in mRNA expression of related genes during Ara-C transport or metabolism. Western blot and RT-PCR were used to detect SAMHD1 expression after regulating <i>DYRK1A</i> expression in Ara-C treated cells. Co-IP technology was used to detect the interaction between Cyclin L2, <i>DYRK1A</i>, and SAMHD1.</p><p><strong>Results: </strong>Overexpression of <i>DYRK1A</i> decreased Ara-C sensitivity in THP-1 cells while silencing <i>DYRK1A</i> increased it. Overexpression and silencing of <i>DYRK1A</i> did not affect Ara-C transport or metabolic gene expression. Overexpression of <i>DYRK1A</i> could increase the expression of SAMHD1 protein in cells, while silencing <i>DYRK1A</i> reduced SAMHD1 expression. Cyclin L2 interacted with <i>DYRK1A</i> and SAMHD1 in THP-1 cells.</p><p><strong>Conclusion: </strong><i>DYRK1A</i> is involved in Ara-C resistance in AML cells, and its mechanism may be related to increased expression of SAMHD1 by interacting with Cyclin L2.</p>","PeriodicalId":35777,"journal":{"name":"中国实验血液学杂志","volume":"33 3","pages":"648-652"},"PeriodicalIF":0.0000,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"[Mechanism of <i>DYRK1A</i> in Cytarabine Resistance in Acute Myeloid Leukemia].\",\"authors\":\"Jia-Wei Feng, Hong-Juan Yu\",\"doi\":\"10.19746/j.cnki.issn.1009-2137.2025.03.004\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objective: </strong>To investigate the role of <i>DYRK1A</i> in the cytarabine (Ara-C) resistance mechanism of acute myeloid leukemia (AML) cells.</p><p><strong>Methods: </strong>Overexpression and silencing of <i>DYRK1A</i> gene in THP-1 cells were used to observe whether the sensitivity of THP-1 cells to Ara-C was altered. RT-PCR was used to detect the changes in mRNA expression of related genes during Ara-C transport or metabolism. Western blot and RT-PCR were used to detect SAMHD1 expression after regulating <i>DYRK1A</i> expression in Ara-C treated cells. Co-IP technology was used to detect the interaction between Cyclin L2, <i>DYRK1A</i>, and SAMHD1.</p><p><strong>Results: </strong>Overexpression of <i>DYRK1A</i> decreased Ara-C sensitivity in THP-1 cells while silencing <i>DYRK1A</i> increased it. Overexpression and silencing of <i>DYRK1A</i> did not affect Ara-C transport or metabolic gene expression. Overexpression of <i>DYRK1A</i> could increase the expression of SAMHD1 protein in cells, while silencing <i>DYRK1A</i> reduced SAMHD1 expression. Cyclin L2 interacted with <i>DYRK1A</i> and SAMHD1 in THP-1 cells.</p><p><strong>Conclusion: </strong><i>DYRK1A</i> is involved in Ara-C resistance in AML cells, and its mechanism may be related to increased expression of SAMHD1 by interacting with Cyclin L2.</p>\",\"PeriodicalId\":35777,\"journal\":{\"name\":\"中国实验血液学杂志\",\"volume\":\"33 3\",\"pages\":\"648-652\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2025-06-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"中国实验血液学杂志\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.19746/j.cnki.issn.1009-2137.2025.03.004\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"Medicine\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"中国实验血液学杂志","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.19746/j.cnki.issn.1009-2137.2025.03.004","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"Medicine","Score":null,"Total":0}
[Mechanism of DYRK1A in Cytarabine Resistance in Acute Myeloid Leukemia].
Objective: To investigate the role of DYRK1A in the cytarabine (Ara-C) resistance mechanism of acute myeloid leukemia (AML) cells.
Methods: Overexpression and silencing of DYRK1A gene in THP-1 cells were used to observe whether the sensitivity of THP-1 cells to Ara-C was altered. RT-PCR was used to detect the changes in mRNA expression of related genes during Ara-C transport or metabolism. Western blot and RT-PCR were used to detect SAMHD1 expression after regulating DYRK1A expression in Ara-C treated cells. Co-IP technology was used to detect the interaction between Cyclin L2, DYRK1A, and SAMHD1.
Results: Overexpression of DYRK1A decreased Ara-C sensitivity in THP-1 cells while silencing DYRK1A increased it. Overexpression and silencing of DYRK1A did not affect Ara-C transport or metabolic gene expression. Overexpression of DYRK1A could increase the expression of SAMHD1 protein in cells, while silencing DYRK1A reduced SAMHD1 expression. Cyclin L2 interacted with DYRK1A and SAMHD1 in THP-1 cells.
Conclusion: DYRK1A is involved in Ara-C resistance in AML cells, and its mechanism may be related to increased expression of SAMHD1 by interacting with Cyclin L2.
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