FOXO3 suppresses lymphoma progression through promoting miR-34b/HSPG2 axis

IF 2.2 4区 医学 Q3 HEMATOLOGY International Journal of Laboratory Hematology Pub Date : 2024-05-22 DOI:10.1111/ijlh.14310
Shi Tao, Qianlei Huang, Weilun Zhou, Jing Chen, Yuxuan Man, Lang Chen, Yu Chen
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Abstract

Background

Diffuse large B-cell lymphoma (DLBCL) is the most common type of lymphoma, which caused many patients to lose their precious lives. FOXO3 was a suppressor in various cancers, however, the role and mechanism of FOXO3 in DLBCL remain unclear.

Methods

Bioinformatics analysis was used to offer information FOXO3 expression and its expression for prognosis of DLBCL patients. The abundance of genes and proteins was evaluated using RT-qPCR and western blot. Cell proliferation and apoptosis was detected by CCK-8 and flow cytometry. The interactions among FOXO3, miR-34b, and HSPG2 were predicted by TransmiR and Starbase and validated using dual luciferase reporter assay, ChIP assay, and RIP assay.

Results

Our findings revealed that FOXO3 expression was abnormally declined in DLBCL cells. FOXO3 upregulation restrained cell proliferation and promoted cell apoptosis of DLBCL cells, while miR-34b inhibitor eliminated these influences. Similarly, miR-34b mimic suppressed malignant behaviors of DLBCL cells, which were abolished by HSPG2 overexpression. Mechanically, FOXO3 induced miR-34b expression through interacting with miR-34b promoter and HSPG2 was a targeted gene of miR-34b.

Conclusion

FOXO3 attenuated the capability of cell proliferation and promoted cell apoptosis rate of DLBCL cells through affecting miR-34b/HSPG2 axis, therefore inhibiting DLBCL progression.

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FOXO3 通过促进 miR-34b/HSPG2 轴抑制淋巴瘤进展
背景:弥漫大 B 细胞淋巴瘤(DLBCL弥漫大B细胞淋巴瘤(DLBCL)是最常见的淋巴瘤类型,它使许多患者失去了宝贵的生命。FOXO3是多种癌症的抑制因子,然而,FOXO3在DLBCL中的作用和机制仍不清楚:方法:利用生物信息学分析提供 FOXO3 的表达及其对 DLBCL 患者预后的影响。采用 RT-qPCR 和 Western 印迹技术评估了基因和蛋白质的丰度。CCK-8和流式细胞术检测了细胞的增殖和凋亡。TransmiR和Starbase预测了FOXO3、miR-34b和HSPG2之间的相互作用,并使用双荧光素酶报告实验、ChIP实验和RIP实验进行了验证:结果:我们的研究结果表明,FOXO3在DLBCL细胞中的表达异常下降。FOXO3的上调抑制了DLBCL细胞的增殖并促进了细胞凋亡,而miR-34b抑制剂则消除了这些影响。同样,miR-34b模拟物抑制了DLBCL细胞的恶性行为,而HSPG2的过表达则消除了这些行为。从机理上讲,FOXO3通过与miR-34b启动子相互作用诱导miR-34b的表达,而HSPG2是miR-34b的靶基因:结论:FOXO3通过影响miR-34b/HSPG2轴,减弱了DLBCL细胞的增殖能力,促进了细胞凋亡率,从而抑制了DLBCL的进展。
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来源期刊
CiteScore
4.50
自引率
6.70%
发文量
211
审稿时长
6-12 weeks
期刊介绍: The International Journal of Laboratory Hematology provides a forum for the communication of new developments, research topics and the practice of laboratory haematology. The journal publishes invited reviews, full length original articles, and correspondence. The International Journal of Laboratory Hematology is the official journal of the International Society for Laboratory Hematology, which addresses the following sub-disciplines: cellular analysis, flow cytometry, haemostasis and thrombosis, molecular diagnostics, haematology informatics, haemoglobinopathies, point of care testing, standards and guidelines. The journal was launched in 2006 as the successor to Clinical and Laboratory Hematology, which was first published in 1979. An active and positive editorial policy ensures that work of a high scientific standard is reported, in order to bridge the gap between practical and academic aspects of laboratory haematology.
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