MiR-133 促进急性髓性白血病细胞(HL-60/ADR)对多诺比星的耐药性

IF 4.6 Q2 MATERIALS SCIENCE, BIOMATERIALS
Lin Liu, Kun Yu, Jingxing Yu, Wei Tao, Yueping Wei
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引用次数: 0

摘要

本研究旨在探索miR-133在急性髓性白血病(AML)多药耐药性中的作用和分子机制,为AML患者的治疗和预后提供新的理论依据。我们进行了细胞水平的实验。我们使用 RT-qPCR 和 Western 印迹法检测基因和蛋白的表达;使用 CCK-8 检测法测量细胞活力;使用流式细胞仪检测细胞凋亡;使用双荧光素酶报告基因检测法验证 miR-133 和 CXCL12 之间的结合。本研究发现,miR-133 在 HL-60/ADR 耐多药细胞中上调。从功能上讲,抑制 miR-133 可以缓解 HL-60/ADR 细胞对 daunorubicin(DNR)的耐药性。在用 DNR 处理的 HL-60/ADR 细胞中抑制 miR-133 后,细胞内耐药相关蛋白 MRP562 和 P-gp 的表达受到抑制,细胞增殖减少,凋亡增加。从机理上讲,NF-κB 信号通路调控了 miR-133 在 HL-60/ADR 细胞中的表达,而 miR-133 靶向 CXCL12 则增强了 HL-60/ADR 细胞对 DNR 的耐药性。总之,NF-κB信号通路调控miR-133的表达,抑制miR-133的表达可以靶向CXCL12,提高HL-60/ADR细胞对DNR的敏感性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

MiR-133 promotes the multidrug resistance of acute myeloid leukemia cells (HL-60/ADR) to daunorubicin

MiR-133 promotes the multidrug resistance of acute myeloid leukemia cells (HL-60/ADR) to daunorubicin

This study aimed to explore the role and molecular mechanism of miR-133 in multidrug resistance in acute myeloid leukemia (AML) and provide a new theoretical basis for the treatment and prognosis of AML patients. We performed experiments at the cellular level. RT‒qPCR and Western blotting were used to detect gene and protein expression; cell viability was measured with CCK-8 assays; apoptosis was detected via flow cytometry; and a dual-luciferase reporter gene assay was used to verify the binding between miR-133 and CXCL12. In this study, we found that miR-133 was upregulated in HL-60/ADR multidrug-resistant cells. Functionally, the inhibition of miR-133 alleviated the resistance of HL-60/ADR cells to daunorubicin (DNR). After inhibiting miR-133 in HL-60/ADR cells treated with DNR, the expression of the intracellular drug resistance-related proteins MRP562 and P-gp was inhibited, cell proliferation decreased, and apoptosis increased. Mechanistically, the NF-κB signaling pathway regulates the expression of miR-133 in HL-60/ADR cells, and the targeting of CXCL12 by miR-133 enhances the resistance of HL-60/ADR cells to DNR. In conclusion, the NF-κB signaling pathway regulates the expression of miR-133, and inhibiting miR-133 expression can target CXCL12 to increase the sensitivity of HL-60/ADR cells to DNR.

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来源期刊
ACS Applied Bio Materials
ACS Applied Bio Materials Chemistry-Chemistry (all)
CiteScore
9.40
自引率
2.10%
发文量
464
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