<br>LncRNA LBX2-AS1 通过 miR-455-5p/MYLIP 轴抑制急性髓系白血病进展,Heliyon

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LncRNA LBX2-AS1 通过 miR-455-5p/MYLIP 轴抑制急性髓系白血病进展
Heliyon ( IF 3.4 ) Pub Date : 2024-01-19 , DOI: 10.1016/j.heliyon.2024.e24812
Gongli Fu ₁ , Hao Wu ₁ , Xiaomiao Wu ₁ , Yang Yang ₂ , Cuihua Fan ₁

Affiliation

急性髓性白血病（AML）是一种常见的血癌，主要影响骨髓和血细胞，在成人中普遍存在。长链非编码 RNA （lncRNA）已被证明在 AML 的发生和发展中起着至关重要的作用。LBX2-AS1 是最近发现的一种 lncRNA，与多种癌症的发病机制和进展有关。本研究旨在探讨 LBX2-AS1 在 AML 中的作用和可能机制。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。分别通过细胞计数试剂盒-8 和 5-乙炔基-2′-脱氧尿嘧啶测定和流式细胞术测定细胞增殖和凋亡。LBX2-AS1 在 AML 标本和细胞中下调，LBX2-AS1 过表达在体外显著抑制细胞增殖并增强细胞凋亡。我们还通过体内生物发光成像确定了 LBX2-AS1 过表达在 AML 小鼠模型中的影响。从机制上讲，LBX2-AS1 充当竞争性内源性 RNA，它通过海绵 miR-455-5p 促进肌球蛋白调节轻链相互作用蛋白（MYLIP）的表达。敲除 MYLIP 或上调 miR-455-5p 拮抗 LBX2-AS1 过表达对 AML 进展的影响。因此，LBX2-AS1 可能是 AML 的有价值的治疗靶点。

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LncRNA LBX2-AS1 inhibits acute myeloid leukemia progression through miR-455-5p/MYLIP axis

Acute myeloid leukemia (AML) is a common blood cancer primarily affecting the bone marrow and blood cells, which is prevalent among adults. Long non-coding RNAs (lncRNAs) have been shown to play a crucial role in the development and progression of AML. 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. Cell proliferation and apoptosis were determined by Cell Counting Kit-8 and 5-ethynyl-2′-deoxyuridine assays, and flow cytometry, respectively. LBX2-AS1 was downregulated in AML specimens and cells, and overexpression of LBX2-AS1 significantly inhibited cell proliferation and enhanced apoptosis in vitro. We also determined the effects of LBX2-AS1 overexpression in an AML mouse model by in vivo bioluminescence imaging. Mechanistically, LBX2-AS1 acts as a competitive endogenous RNA, which promotes myosin regulatory light chain interacting protein (MYLIP) expression by sponging miR-455-5p. Knockdown of MYLIP or upregulation of miR-455-5p antagonized the effect of LBX2-AS1 overexpression on the progression of AML. LBX2-AS1 may thus be a valuable therapeutic target for AML.

更新日期：2024-01-19

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