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Published in: Indian Journal of Hematology and Blood Transfusion 2/2021

01-04-2021 | Acute Myeloid Leukemia | Original Article

Downregulation of MIR100HG Induces Apoptosis in Human Megakaryoblastic Leukemia Cells

Authors: Parisa Bagheri, Mohammadreza Sharifi, Ava Ghadiri

Published in: Indian Journal of Hematology and Blood Transfusion | Issue 2/2021

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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.
Literature
Metadata
Title
Downregulation of MIR100HG Induces Apoptosis in Human Megakaryoblastic Leukemia Cells
Authors
Parisa Bagheri
Mohammadreza Sharifi
Ava Ghadiri
Publication date
01-04-2021
Publisher
Springer India
Published in
Indian Journal of Hematology and Blood Transfusion / Issue 2/2021
Print ISSN: 0971-4502
Electronic ISSN: 0974-0449
DOI
https://doi.org/10.1007/s12288-020-01324-6

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