ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2020
Reduce proliferation of human bone marrow cells from acute myeloblastic leukemia with minimally differentiation by blocking lncRNA PVT1.
Article in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Antisense LNA GapmeR targeting hsa-piR-33195 induces antiproliferative and apoptotic effects on human acute myeloid leukemia.Medical oncology (Northwood, London, England) · 2025Article
- lncRNA PVT1: a novel oncogene in multiple cancers.Cellular & molecular biology letters · 2022Review
- S100A8 inhibition in leukemic lymphoblasts induces sensitivity to chemotherapy and inhibition of disease relapse.Medical oncology (Northwood, London, England) · 2022Article
- Article
- Knockdown of SOX12 Expression Induced Apoptotic Factors is Associated with TWIST1 and CTNNB1 Expression in Human Acute Myeloid Leukemia Cells.International journal of molecular and cellular medicine · 2021Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
purposeAcute 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.
methodsIn 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.
resultsThe 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.
conclusionThe 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.
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