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The Effect of Decitabine on the Expression and Methylation of the Ppp1ca, Btg2, and Pten in Association With Changes in Mir-125B, Mir-17, and Mir-181B in Nalm6 Cell Line Publisher Pubmed



Vafadar A1 ; Mokaram P2 ; Erfani M2 ; Yousefi Z3 ; Farhadi A4 ; Elham Shirazi T5 ; Tamaddon G4
Authors
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Authors Affiliations
  1. 1. Department of Medical Biotechnology, School of Paramedical Sciences, Shiraz University of Medical Sciences, Shiraz, Iran
  2. 2. Department of Biochemistry, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran
  3. 3. Department of Immunology, Faculty of Medicine, Isfahan University of Medical Science, Isfahan, Iran
  4. 4. Diagnostic Laboratory Sciences and Technology Research Center, School of Paramedical Sciences, Shiraz University of Medical Sciences, Shiraz, Iran
  5. 5. Department of Pharmacology & Toxicology, School of Pharmacy, Shiraz University of Medical Sciences, Shiraz, Iran

Source: Journal of Cellular Biochemistry Published:2019


Abstract

Precursor B-cell acute lymphoblastic leukemia (B-ALL) is the most prevalent pediatric cancer. DNA methylation and changes in the microRNAs (miRNAs) expression are known to be important causes of B-ALL. Decitabine as a DNA methyltransferase inhibitor agent is able to induce hypomethylation in several tumor suppressor genes. Much evidence has proven BTG2, PPP1CA, and PTEN act as tumor suppressor genes in many malignancies. In this case control study, the messenger RNA (mRNA) expression of PPP1CA, BTG2, and PTEN genes using quantitative real-time polymerase chain reaction (rRT-PCR) in Nalm6 cell line and five patients suffer from ALL with mean age 5.6 years were determined in compare with seven normal healthy donors age and sex matched. qRT-PCR analysis revealed that the expression levels of PPP1CA, BTG2, and PTEN genes were significantly decreased in Nalm6 ([FC] = 0.46, [FC] = 0.046, [FC] = 0.54) and according to the Methylation-specific PCR (MSP) analysis, these genes were hypermethylated in Nalm6. In next step, the effects of decitabine treatment on the methylation and expression of these genes in association with changes in miR-125b, miR-17, and miR-181b expression levels were evaluated in optimal concentration 2.5 µM of decitabine. Our data showed that decitabine is able to restore the expression levels of aforementioned genes and downregulate expression levels of oncomiRs; including miR-125b, miR-17, and miR-181b in Nalm6 cell line. Therefore, it seems that decitabine can be used as a potential drug for the first line treatment of patients with B-ALL, but further in vivo investigation is necessary. © 2019 Wiley Periodicals, Inc.
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