ABSTRACT
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.
Subject(s)
Bone Marrow Cells/physiology , Leukemia, Myeloid, Acute/pathology , RNA, Long Noncoding/antagonists & inhibitors , Apoptosis , Cell Differentiation , Cell Proliferation , Cells, Cultured , Humans , Leukemia, Myeloid, Acute/drug therapy , Proto-Oncogene Proteins c-myc/physiology , RNA, Long Noncoding/metabolismABSTRACT
BACKGROUND: Chronic myeloid leukemia (CML), is the first malignancy that related to the chromosomal abnormality and include 15-20% of all adulthood leukemia. AIMS: This study aimed to compare the hematologic, breakpoint cluster region-abelson (BCR-ABL) and liver function enzymes changes during treatment period of Imatinib. SETTINGS AND DESIGN: A noncurrent clinical trial study. MATERIALS AND METHODS: New incident CML patients received Iranian made or Indian-made Imatinib after baseline measurement. Hematologic, BCR-ABL, electrolytes and liver function enzymes measured again after 24 weeks. STATISTICAL ANALYSIS USED: Paired t-test and independent t-test was used to assess the effect of treatment in within and between groups, respectively. RESULTS: Imatinib has a decreasing impact on white blood cells and placates. While an increasing effect on hemoglobin concentration. Iranian made and Indian-made Imatinib has a same effect on improvement of hematologic, BCR-ABL, electrolytes in CML patients. However, the liver changes of Imatinib were not clinically significant. CONCLUSION: The Iranian-made Imatinib can be used as a replacement for Indian made ones without any statistical and clinical significant difference on Improvement of CML patients.
