Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:2.7.7.49 (
reverse transcriptase
)
31,746
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
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.
...
PMID: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. 3014 68