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MIR100HG的下调诱导人巨核母细胞白血病细胞凋亡。

Downregulation of MIR100HG Induces Apoptosis in Human Megakaryoblastic Leukemia Cells.

作者信息

Bagheri Parisa, Sharifi Mohammadreza, Ghadiri Ava

机构信息

Department of Genetics and Molecular Biology, School of Medicine, Isfahan University of Medical Science, Isfahan, 81744-176 Iran.

出版信息

Indian J Hematol Blood Transfus. 2021 Apr;37(2):232-239. doi: 10.1007/s12288-020-01324-6. Epub 2020 Jul 24.

DOI:10.1007/s12288-020-01324-6
PMID:33867729
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8012473/
Abstract

Long noncoding ribonucleic acids (lncRNAs) are ribonucleic acid (RNA) molecules longer than 200 nucleotides without protein-coding capacity. Several studies have shown that lncRNAs play a pivotal role in the initiation, maintenance, and progression of acute myeloid leukemia (AML), which could make them a promising candidate in the diagnosis and treatment of leukemia. Acute Megakaryoblastic leukemia (AMKL) is a rare form of AML with a poor prognosis and low survival. It has been reported that lncRNA MIR100HG is involved several types of malignancies. In the present study, MIR100HG was downregulated in a human acute megakaryoblastic leukemia cell line (M-07e) using Antisense LNA GapmeRs. In order to assess the expression level of MIR100HG, cell viability, apoptosis, and necrosis (late apoptosis), quantitative reverse transcription polymerase chain reaction (qRT-PCR), Methyl-thiazol Tetrazolium assay, AnnexinV, and propidium iodide staining was performed at different time points after the transfection. In addition, the expression level of TGFβ was evaluated by qRT-PCR. Our results revealed that inhibition of MIR100HG might serve as a new method for inhibition of the proliferation of AMKL cells and therefore, could be a promising approach in medicine for targeted therapy in AMKL.

摘要

长链非编码核糖核酸(lncRNAs)是长度超过200个核苷酸且无蛋白质编码能力的核糖核酸(RNA)分子。多项研究表明,lncRNAs在急性髓系白血病(AML)的发生、维持和进展中起关键作用,这使其有望成为白血病诊断和治疗的候选靶点。急性巨核细胞白血病(AMKL)是AML的一种罕见形式,预后较差,生存率低。据报道,lncRNA MIR100HG与多种恶性肿瘤有关。在本研究中,使用反义锁核酸GapmeRs在人急性巨核细胞白血病细胞系(M-07e)中下调MIR100HG。为了评估MIR100HG的表达水平、细胞活力、凋亡和坏死(晚期凋亡),在转染后的不同时间点进行了定量逆转录聚合酶链反应(qRT-PCR)、甲基噻唑四氮唑法、膜联蛋白V和碘化丙啶染色。此外,通过qRT-PCR评估TGFβ的表达水平。我们的结果表明,抑制MIR100HG可能是抑制AMKL细胞增殖的一种新方法,因此,可能是AMKL靶向治疗的一种有前景的医学方法。

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Onco Targets Ther. 2019 Apr 17;12:2967-2973. doi: 10.2147/OTT.S202528. eCollection 2019.
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Biosci Rep. 2019 Apr 5;39(4). doi: 10.1042/BSR20190171. Print 2019 Apr 30.
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Int J Mol Sci. 2019 Feb 9;20(3):735. doi: 10.3390/ijms20030735.
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