2023年12月1日 · Our results confirmed that miR-455-3p is expressed at low levels in AML, and overexpression of miR-455-3p promoted cell cycle arrest in the G0/G1 phase, affected cell cycle progression, inhibited cell proliferation, and promoted apoptosis and autophagy.

miR-455-3p在外周血和AML细胞系中显着减少， UBN2表现出高表达。 转染的miR-455-3p模拟物有效地抑制了AML细胞的活性，而UBN2的过表达或添加自噬抑制剂CQ则逆转了miR-455-3p的作用。

2024年1月30日 · We assessed how LBX2-AS1 relied on miR-455-5p to affect cell proliferation and apoptosis in AML cells by co-transfecting OE-LBX2-AS1 plasmids and miR-455-5p mimics into MOLM-13 and HL-60 cells. The results revealed that the miR-455-5p mimic was able to reverse the overexpression level of LBX2-AS1 by RT-qPCR ( Fig. 4 A).

2024年1月1日 · LBX2-AS1 is a recently discovered lncRNA that has been linked to the pathogenesis and progression of several types of cancer. This study aimed to investigate the role and possible mechanisms of LBX2-AS1 in AML. Expression levels of LBX2-AS1, miR-455-5p, and their target genes were detected in AML samples and cells by RT-qPCR.

该论文旨在研究lbx2-as1在aml中的作用和可能的机制。 研究人员通过RT-qPCR检测AML样本和细胞中LBX2-AS1、miR-455-5p及其靶基因的表达水平。 细胞增殖和凋亡分别通过细胞计数试剂盒-8和5-乙炔基-2'-脱氧尿嘧啶分析和流式细胞术进行确定。

Overexpression of miR-455-3p facilitates apoptosis and autoph- agy in acute myeloid leukemia (AML) cells. miR-455-3p affects the progression of AML through UBN2.

2024年1月19日 · LBX2-AS1 is a recently discovered lncRNA that has been linked to the pathogenesis and progression of several types of cancer. This study aimed to investigate the role and possible mechanisms of LBX2-AS1 in AML. Expression levels of LBX2-AS1, miR-455-5p, and their target genes were detected in AML samples and cells by RT-qPCR.

本研究旨在探讨lbx2-as1在aml中的作用及可能机制。 通过 RT-qPCR 检测 AML 样本和细胞中 LBX2-AS1、miR-455-5p 及其靶基因的表达水平。 分别通过 Cell Counting Kit-8 和 5-ethynyl-2'-deoxyuridine 测定以及流式细胞术测定细胞增殖和凋亡。

Our results confirmed that miR-455-3p is expressed at low levels in AML, and overexpression of miR-455-3p promoted cell cycle arrest in the G0/G1 phase, affected cell cycle progression, inhibited cell proliferation, and promoted apoptosis and autophagy.

The transfected miR-455-3p mimic effectively restrained the activity of AML cells, whereas overexpression of UBN2 or the addition of the autophagy inhibitor CQ reversed the effect of miR-455-3p. The interaction between UBN2 and peroxisome proliferator-activated receptor alpha (PPARα) was confirmed by coimmunoprecipitation, and overexpression ...