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Updated: Dec 21, 2025
Pan-myeloid Differentiation of Human Cord Blood Derived CD34+ Hematopoietic Stem and Progenitor Cells
Published on: August 9, 2019
Reduce proliferation of human bone marrow cells from acute myeloblastic leukemia with minimally differentiation by
Purpose:
Acute myeloblastic leukemia with minimally differentiation (AML-M0) is a subtype of acute leukemia with poor prognosis. The recent studies have shown that long non-coding RNAs (lncRNAs) play an important role in different cellular processes, such as cell cycle control and proliferation. Plasmacytoma variant translocation 1 (PVT1) is one of those lncRNAs that is significantly upregulated in AML. LncRNAs could be downregulated or blocked by locked nucleic acids (LNA) which are oligonucleotide strands.
Methods:
In this study, lncRNA PVT1 was blocked by antisense LNA GapmeRs in human bone marrow cancerous blast cells. Cells were transfected with PVT1 antisense LNA GapmeRs at 24, 48, and 72 h post-transfection. Quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) was accomplished to evaluate the PVT1 and c-Myc expression. Cell viability was evaluated by MTT assay, and apoptosis and necrosis were assessed by Annexin V/propidium iodide staining assay.
Results:
The results of this study indicated that the downregulation of PVT1 in blast cells could induce apoptosis, and necrosis and reduce cell viability. The expression of c-Myc was downregulated by blockage of PVT1 and it shows that the expression of these two genes are correlated.
Conclusion:
The findings declare that inhibition of PVT1 could be a new target in the treatment of AML-M0 and help to approach more to treatments with fewer side effects.
Insights
Inhibition of the long non-coding RNA PVT1 in acute myeloid leukemia (AML-M0) cells reduced cell viability and induced apoptosis. Blocking PVT1 also downregulated c-Myc, suggesting PVT1 as a potential therapeutic target for AML-M0.
Area of Science:
- Oncology
- Molecular Biology
- Gene Regulation
Background:
- Acute myeloid leukemia with minimally differentiated (AML-M0) has a poor prognosis.
- Long non-coding RNAs (lncRNAs) regulate crucial cellular processes like proliferation.
- Plasmacytoma variant translocation 1 (PVT1) is a lncRNA upregulated in AML.
Purpose of the Study:
- To investigate the effect of blocking lncRNA PVT1 using locked nucleic acid (LNA) GapmeRs in AML-M0 cells.
- To assess the impact of PVT1 inhibition on cell viability, apoptosis, and necrosis.
- To determine the correlation between PVT1 and c-Myc expression.
Main Methods:
- Human bone marrow blast cells from AML-M0 patients were transfected with PVT1 antisense LNA GapmeRs.
- Quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) was used to measure PVT1 and c-Myc expression.
- Cell viability was assessed using MTT assay, and apoptosis/necrosis were evaluated by Annexin V/propidium iodide staining.
Main Results:
- Downregulation of PVT1 in blast cells led to increased apoptosis and necrosis.
- PVT1 inhibition significantly reduced cell viability.
- Blocking PVT1 resulted in decreased c-Myc expression, indicating a correlation between the two.
Conclusions:
- Inhibition of lncRNA PVT1 represents a promising therapeutic strategy for AML-M0.
- Targeting PVT1 may lead to novel treatments for AML-M0 with potentially fewer side effects.
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