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Transcription Analysis of a Histones Modifiers Panel Coupled With Critical Tumor Suppressor Genes Displayed Frequent Changes in Patients With Aml.: Mrna Levels of Histones Modifiers and Tsgs in Aml Publisher Pubmed



Amiri V1 ; Mohammadi MH1, 2 ; Rafiee M1 ; Ghezelbash B3 ; Salari S4 ; Allahbakhshian Farsani M1, 2
Authors
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Authors Affiliations
  1. 1. Department of Laboratory Hematology and Blood Bank, School of Allied Medical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran
  2. 2. HSCT Research Center, Shahid Beheshti University of medical science, Tehran, Iran
  3. 3. Department of Hematology, School of Medicine, Seyyed Al-Shohada Hospital of Isfahan University of Medical Sciences, Isfahan, Iran
  4. 4. Department of Internal Medicine, Taleghani General Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran

Source: Current Research in Translational Medicine Published:2021


Abstract

Epigenetic alterations could cause leukemia through the activation of normally silent loci or silencing of normally active loci. We herein aimed to compare the expression patterns of a histone modifiers panel consisted of SUV39H1, PRDM16, UHRF2, KDM2B, and KDM3C between acute myeloid leukemia(AML) cells and normal cells and to assess the correlation of these genes with the expression of vital tumor suppressor genes, including p16INK4A and p53. Bone marrow or peripheral blood samples of 50 AML patients at diagnosis and also 18 subjects with a normal hematopoietic system as a control group were obtained after informed consent. Then, qRT-PCR was performed to determine the expression levels of the aforementioned genes. We found a broad alteration in the expression signature of five out of seven studied genes in AML patients as compared with the control group. UHRF2 and p53 were remarkably downregulated in AML patients (P<0.001), while SUV39H1, PRDM16, and KDM3C were significantly overexpressed (P<0.01). Based on the Spearman rank correlation, SUV39H1 and KDM2B negatively regulated both p16INK4A and p53 expression. Taken together, our findings provided preliminary evidence regarding the pervasive mRNA perturbation of histone modifiers and their plausible influences on critical tumor suppressor genes. Future studies in this area would be required to assist in establishing these results in the clinical practice of AML patients. © 2021
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