MicroRNA-765在骨髓增生异常综合征中上调,并通过抑制白血病细胞中的PLP2诱导细胞凋亡。

IF 2.3 Q2 HEMATOLOGY
Blood Research Pub Date : 2023-09-30 Epub Date: 2023-07-27 DOI:10.5045/br.2023.2023097
Seong-Ho Kang, Ji Seon Choi
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引用次数: 0

摘要

背景:表观遗传学研究,特别是对微小RNA(miRNA)的研究已经蓬勃发展。miRNA的异常表达导致血液系统恶性肿瘤的发展。据报道,miR-765通过下调导致细胞凋亡的蛋白脂质蛋白2(PLP2)来抑制细胞增殖。我们研究了骨髓增生异常综合征(MDS)中miR-765的失调。方法:我们比较了65例MDS患者和11例对照组的miR-765表达谱。进行细胞增殖和凋亡测定以确定miR-765对用miR-765模拟物转染的白血病细胞的体外作用。进行逆转录定量PCR(RT-qPCR)和蛋白质印迹来检测miR-765的靶点。结果:我们发现,与对照组相比,MDS患者的miR-765水平上调了10.2倍。在多谱系发育不良的难治性细胞减少症中,miR-765水平升高的患者比例显著高于其他形式的MDS。对白血病细胞的实验显示,用miR-765模拟物转染抑制细胞增殖并诱导细胞凋亡。RT-qPCR和western印迹显示miR-765的靶点是PLP2。结论:这些发现表明miR-765上调通过下调PLP2诱导细胞凋亡,并可能在MDS的发病机制中发挥作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

MicroRNA-765 is upregulated in myelodysplastic syndromes and induces apoptosis via PLP2 inhibition in leukemia cells.

MicroRNA-765 is upregulated in myelodysplastic syndromes and induces apoptosis via PLP2 inhibition in leukemia cells.

MicroRNA-765 is upregulated in myelodysplastic syndromes and induces apoptosis via PLP2 inhibition in leukemia cells.

MicroRNA-765 is upregulated in myelodysplastic syndromes and induces apoptosis via PLP2 inhibition in leukemia cells.

Background: Epigenetic studies, particularly research on microRNA (miRNA), have flourished. The abnormal expression of miRNA contributes to the development of hematologic malignancies. miR-765 has been reported to inhibit cell proliferation by downregulating proteolipid protein 2 (PLP2), which causes apoptosis. We investigated miR-765 dysregulation in myelodysplastic syndromes (MDS).

Methods: We compared the expression profiles of miR-765 in 65 patients with MDS and 11 controls. Cell proliferation and apoptosis assays were performed to determine the in vitro effects of miR-765 on leukemia cells transfected with the miR-765 mimic. Reverse transcription quantitative PCR (RT-qPCR) and western blotting were performed to examine the targets of miR-765.

Results: We found that miR-765 levels were upregulated 10.2-fold in patients with MDS compared to controls. In refractory cytopenia with multilineage dysplasia, the percentage of patients with elevated miR-765 levels was significantly higher than in other forms of MDS. Experiments with leukemia cells revealed that transfection with a miR-765 mimic inhibited cell proliferation and induced apoptosis. RT-qPCR and western blotting demonstrated that the target of miR-765 was PLP2.

Conclusion: These findings imply that upregulation of miR-765 induces apoptosis via downregulation of PLP2 and may have a role in MDS pathogenesis.

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来源期刊
Blood Research
Blood Research HEMATOLOGY-
CiteScore
3.70
自引率
0.00%
发文量
64
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