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基质相互作用分子 1()的敲低通过抑制活性氧物质的活性抑制急性髓性白血病-M5 细胞系的存活。

Knockdown of Stromal Interaction Molecule 1 () Suppresses Acute Myeloblastic Leukemia-M5 Cell Line Survival Through Inhibition of Reactive Oxygen Species Activities.

机构信息

Universiti Sains Malaysia, Advanced Medical and Dental Institute, Department of Biomedical Science, Pulau Pinang, Malaysia

Hadhramout University, Faculty of Medicine and Health Sciences, Department of Basic Medical Sciences, Hadhramout, Yemen

出版信息

Turk J Haematol. 2023 Feb 28;40(1):11-17. doi: 10.4274/tjh.galenos.2022.2022.0246. Epub 2022 Nov 21.

Abstract

OBJECTIVE

This study aimed to investigate the role of the stromal interaction molecule 1 () gene in the survival of the acute myeloblastic leukemia (AML)-M5 cell line (THP-1).

MATERIALS AND METHODS

The effect was assessed via dicersubstrate siRNA-mediated knockdown. The effect of knockdown on the expression of and pathway-related genes and reactive oxygen species (ROS) generation-related genes was tested using real-time polymerase chain reaction. Cellular functions, including ROS generation, cell proliferation, and colony formation, were also evaluated following knockdown.

RESULTS

The findings revealed that knockdown reduced intracellular ROS levels via downregulation of and . These findings were associated with the downregulation of , and was also downregulated, while was upregulated following knockdown. Furthermore, knockdown reduced THP-1 cell proliferation and colony formation.

CONCLUSION

This study has demonstrated the role of in promoting AML cell proliferation and survival through enhanced ROS generation and regulation of AKT/MAPK-related pathways. These findings may help establish as a potential therapeutic target for AML treatment.

摘要

目的

本研究旨在探讨基质相互作用分子 1()基因在急性髓系白血病(AML)-M5 细胞系(THP-1)存活中的作用。

材料和方法

通过 dicer 底物 siRNA 介导的基因敲低来评估作用。使用实时聚合酶链反应测试基因敲低对和通路相关基因以及活性氧(ROS)生成相关基因表达的影响。在基因敲低后,还评估了细胞功能,包括 ROS 生成、细胞增殖和集落形成。

结果

研究结果表明,基因敲低通过下调和来降低细胞内 ROS 水平。这些发现与下调和有关,下调的同时,也上调了,而下调。此外,基因敲低可降低 THP-1 细胞增殖和集落形成。

结论

本研究表明,通过增强 ROS 生成和调节 AKT/MAPK 相关途径,在促进 AML 细胞增殖和存活中发挥作用。这些发现可能有助于将确定为 AML 治疗的潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c64/9979743/1236d319462c/TJH-40-11-g1.jpg

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