Samieyan Dehkordi Sahar, Mousavi Seyed Hadi, Ebrahimi Marzieh, Alizadeh S Haban, Hedayati Asl Amir Abbas, Mohammad Monireh, Aliabedi Bahareh
Department of Hematology, School of Allied Medical Sciences, Tehran University of Medical Sciences, Tehran, Iran.
Department of Hematology, School of Allied Medical Sciences, Tehran University of Medical Sciences, Tehran, Iran. Email:
Cell J. 2022 Feb;24(2):76-84. doi: 10.22074/cellj.2022.7658.
Acute myeloid leukemia (AML) is characterized by abnormalities of differentiation and growth of primary hematopoietic stem cells (HSCs) in the blood and bone marrow. In many studies, miR-625-5p has been shown to inhibit downstream pathways from affecting the metastasis and invasion of the integrin-linked kinase (ILK) signaling pathway. It has been proved that the expression of miR-625-5p decreases in AML cell lines. This study aimed to investigate the effect of miR-625-5p upregulation on the invasion of KG1 ell line .
In this experimental study, we investigated the impact of upregulation of miR-625-5p on invasion via the ILK/AKT pathway in the KG1 cell line. After transfection using the viral method, the cellular invasion was assessed by invasion assay and the levels of miR-625-5p genes and protein were evaluated by quantitative polymerase chain reaction (qPCR) and western blotting. Moreover, CXCR4 level was assessed by flow cytometry.
The invasion significantly reduced in MiR-625-5p-transfected KG1 cells (P<0.01) that was concomitant with remarkably decreasing in the expression levels of and genes compare with the control group (P<0.01). Incontrast, and significantly increased (P<0.01, P<0.001 and P<0.01, respectively) and GSK3β did not change significantly in MiR-625-5p-transfected KG1 cells. The protein level of NF-κB decreased (P<0.01) and MMP9 increased, however it was not significant. Moreoever, the expression of CXCR4 was significantly lower (P<0.01) in comparison with the control group.
miR-625-5p leads to a reduction in cell invasion in the AML cell line through ILK pathway. Therefore, it could be a breakthrough in future AML-related research. However, further studies are needed to support this argument.
急性髓系白血病（AML）的特征是血液和骨髓中原始造血干细胞（HSCs）的分化和生长异常。在许多研究中，miR-625-5p已被证明可抑制下游通路，影响整合素连接激酶（ILK）信号通路的转移和侵袭。已证实miR-625-5p在AML细胞系中的表达降低。本研究旨在探讨上调miR-625-5p对KG1细胞系侵袭的影响。
在本实验研究中，我们通过ILK/AKT通路研究了上调miR-625-5p对KG1细胞系侵袭的影响。采用病毒法转染后，通过侵袭试验评估细胞侵袭能力，并通过定量聚合酶链反应（qPCR）和蛋白质印迹法评估miR-625-5p基因和蛋白质水平。此外，通过流式细胞术评估CXCR4水平。
与对照组相比，转染MiR-625-5p的KG1细胞侵袭能力显著降低（P<0.01），同时 和 基因的表达水平显著降低（P<0.01）。相反，在转染MiR-625-5p的KG1细胞中， 和 显著增加（分别为P<0.01、P<0.001和P<0.01），而GSK3β没有显著变化。NF-κB蛋白水平降低（P<0.01），MMP9增加，但不显著。此外，与对照组相比，CXCR4的表达显著降低（P<0.01）。
miR-625-5p通过ILK通路导致AML细胞系的细胞侵袭减少。因此，它可能是未来AML相关研究的一个突破。然而，需要进一步的研究来支持这一观点。
