阐明circVRK1及其与miR-4428的相互作用在调节急性淋巴细胞白血病（ALL）细胞增殖和凋亡中的作用。体外培养KOCL44 ALL细胞，实验组包括pcDNA、pcDNA-circVRK1、anti-miR-NC 、抗 miR-4428、si-NC、si-circVRK1、pcDNA-circVRK1 miR-NC 和 pcDNA-circVRK1 miR-4428。使用qRT-PCR检测circVRK1和miR-4428的表达水平。 CCK-8测定和流式细胞术分别用于评估细胞增殖和凋亡。采用双荧光素酶报告基因检测来研究 circVRK1 和 miR-4428 之间的相互作用，分组分为 WT-circVRK1 miR-NC、WT-circVRK1 miR-4428、MUT-circVRK1 miR-NC 和 MUT-circVRK1 miR-4428 。 Western blotting检测Ki-67、cleaved caspase-3、cleaved caspase-9蛋白表达水平。与pcDNA组相比，pcDNA-circVRK1组circVRK1表达上调（P<0.05）。与转染pcDNA或anti-miR-NC相比，转染pcDNA-circVRK1或anti-miR-4428导致KOCL44细胞中细胞活力和Ki-67蛋白水平降低（P<0.05），并且细胞凋亡率和细胞凋亡水平升高。裂解的 caspase-3 和裂解的 caspase-9 (P<0.05)。 circVRK1被发现负向调节miR-4428表达，这种效应仅在WT-circVRK1组中观察到。与pcDNA组相比，pcDNA-circVRK1组中miR-4428水平较低（P<0.05），与si-NC组相比，si-circVRK1组中miR-4428水平较高（P<0.05）。与 pcDNA-circVRK1 miR-4428 共转染可增加细胞活力（P<0.05）和 Ki-67 表达（P<0.05），并降低细胞凋亡率以及 cleaved caspase-3 和 cleaved caspase-9 水平（P<0.05）。 0.05）与pcDNA-circVRK1 miR-NC共转染相比。circVRK1过表达降低急性ALL细胞增殖能力，并通过下调miR-4428表达诱导细胞凋亡。© 2024《四川大学学报（医学版）》编辑部版权所有Copyright ©2024 四川大学学报（医学版）编辑部。

To elucidate the role of circVRK1 and its interaction with miR-4428 in regulating proliferation and apoptosis in acute lymphoblastic leukemia (ALL) cells.KOCL44 ALL cells were cultured in vitro, and experimental groups included pcDNA, pcDNA-circVRK1, anti-miR-NC, anti-miR-4428, si-NC, si-circVRK1, pcDNA-circVRK1+miR-NC, and pcDNA-circVRK1+miR-4428. The expression levels of circVRK1 and miR-4428 were detected using qRT-PCR. CCK-8 assays and flow cytometry were used to assess cell proliferation and apoptosis, respectively. The dual luciferase reporter assays were employed to investigate the interaction between circVRK1 and miR-4428, with groups categorized as WT-circVRK1+miR-NC, WT-circVRK1+miR-4428, MUT-circVRK1+miR-NC, and MUT-circVRK1+ miR-4428. Western blotting was utilized to detect the expression levels of Ki-67, cleaved caspase-3, and cleaved caspase-9 proteins.Compared to the pcDNA group, circVRK1 expression was up-regulated in the pcDNA-circVRK1 group (P<0.05). Compared to transfection with pcDNA or anti-miR-NC, transfection with pcDNA-circVRK1 or anti-miR-4428 led to decreased cell viability and Ki-67 protein levels in KOCL44 cells (P<0.05), and increased apoptosis rates and levels of cleaved caspase-3 and cleaved caspase-9 (P<0.05). circVRK1 was found to negatively regulate miR-4428 expression, with this effect observed only in the WT-circVRK1 group. miR-4428 levels were lower in the pcDNA-circVRK1 group compared to the pcDNA group (P<0.05) and higher in the si-circVRK1 group compared to the si-NC group (P<0.05). Co-transfection with pcDNA-circVRK1+miR-4428 resulted in increased cell viability (P<0.05) and Ki-67 expression (P<0.05), and decreased apoptosis rates and levels of cleaved caspase-3 and cleaved caspase-9 (P<0.05) compared to co-transfection with pcDNA-circVRK1+miR-NC.Overexpression of circVRK1 reduces the proliferation ability of acute ALL cells and induces cell apoptosis by downregulating miR-4428 expression.© 2024《四川大学学报（医学版）》编辑部 版权所有Copyright ©2024 Editorial Office of Journal of Sichuan University (Medical Sciences).