Knockdown of Long Noncoding RNA Plasmacytoma Variant Translocation 1 with Antisense Locked Nucleic Acid GapmeRs Exerts Tumor-Suppressive Functions in Human Acute Erythroleukemia Cells Through Downregulation of C-MYC Expression.

Abstract

Objective: Acute erythroleukemia (AEL) is a subtype of acute myeloid leukemia (AML), with no specific treatment. Up- or downregulation of long noncoding RNAs (lncRNAs) is strongly associated with the formation and progression of many malignancies. Plasmacytoma variant translocation 1 (PVT1) is a significantly upregulated lncRNA in AML. Antisense locked nucleic acid (LNA) GapmeRs oligonucleotides are the novel tools for targeting lncRNAs. The purpose of the current study was to investigate the functional role of PVT1 antisense LNA GapmeRs on AEL cell line (KG-1). Materials and Methods: AEL cells were transfected with PVT1 antisense LNA GapmeRs at three different time points. Quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) was accomplished to evaluate the PVT1 expression by PVT1 antisense LNA GapmeRs. The viability was evaluated by MTT (3-[4, 5-dimethylthiazol-2-yl]-2, 5-diphenyl tetrazolium bromide) assay, and the apoptosis and necrosis were assessed by Annexin V/propidium iodide staining assay. The C-MYC expression level, the target gene of PVT1, was also quantified by qRT-PCR. Results: The results indicated that PVT1 inhibition could significantly decrease the viability of AEL cells, due to induction of apoptosis and necrosis, probably through the downregulation of C-MYC. Conclusions: Their findings suggest that the inhibition of lncRNA PVT1 could serve as a novel approach for controlling the proliferation of AEL cells and could open up a path for treatment of AEL.