The Effect of Long Non-Coding RNA PVT1 Inhibition by Antisense LNA GapmeRs Technology on Proliferation of Human Acute Erythroleukemia Cells

Long non-coding RNAs (LncRNAs) are a class of RNA molecules with 200-10000 nucleotides in length that have lost their protein coding capacity. They play important role in numerous biological processes including cell proliferation, differentiation, apoptosis, and cancer development. Acute myeloid leukemia (AML) is the most common leukemia. Evidence has shown that long non-coding RNAs PVT1 is upregulated in acute myeloid leukemia, and leads to an increase in cell proliferation. This study aimed to assess the effect of long non-coding RNA PVT1 inhibition by antisense LNA GapmeRs technology on proliferation of human acute erythroleukemia cells.
Human acute erythroleukemia cells (KG1), known as subgroup six of acute myeloid leukemia based on the French–American–British (FAB) classification, were cultured in Roswell Park Memorial Institute (RPMI) medium. Long non-coding RNA PVT1 degradation was performed using antisense LNA GapmeRs technology. At different time points after transfection (24, 48, and 72 hours), long non-coding RNA PVT1 expression and cell proliferation were assessed. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was accomplished to evaluate the long non-coding RNAPVT1 expression. Moreover, Cell viability was measured using 3-[4, 5-dimethylthiazol-2-yl]-2, 5-diphenyl tetrazolium bromide (MTT) assay.
Findings: Long non-coding RNA PVT1 expression decreased at 24, 48, and 72 hours after transfection in the antisense LNA GapmeRs group compared to control groups. Cell viability and proliferation was significantly decreased in antisense LNA GapmeRs transfected group compared with other two groups.
The present survey exhibited that inhibition of long non-coding PVT1 by using antisense LNA GapmeRs can dramatically reduce the proliferation of human acute erythroleukemia cells. Our results can be helpful in translational medicine for antisense therapy in acute myeloid leukemia.