[Effects of uroacitides on the methylation of PTEN gene in myelodysplastic syndrome cells and its mechanism]

Zhonghua Xue Ye Xue Za Zhi. 2013 Jul;34(7):600-5. doi: 10.3760/cma.j.issn.0253-2727.2013.07.009.
[Article in Chinese]

Abstract

Objective: To investigate the methylation patterns of PTEN gene in myelodysplastic syndrome (MDS) cell line MUTZ-1 cells and the primary cells, to explore the effects of uroacitides (CDA- II) on the methylation patterns, and to provide novel target therapy for MDS.

Methods: Reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blot were used to determine the expression of PTEN and DNA methyltransferases (DNMTs) as well as the effects of CDA-II on them. Methylation specific PCR (MSP) was used to identify the methylation patterns of PTEN and the effects of CDA-II on them.

Results: PTEN was completely methylated in high-risk MDS and acute myeloid leukemia (AML) transformed from MDS. High expressions of DNMTs proteins, especially DNMT3b protein were found in high-risk MDS and AML cells transformed from MDS. PTEN expression level was increased from 0.02 ± 0.01 at control group to 0.23 ± 0.11, 0.54 ± 0.11 and 0.92 ± 0.13 after treatment with CDA-II at 2, 4 and 8 mg/ml (P<0.01). If the cells were treated with CDA-II at 4 mg/ml for 12, 24 and 48 hours, PTEN expression level was up- regulated to 0.15 ± 0.06, 0.52 ± 0.12 and 0.89 ± 0.13, which were significantly higher than that of control group 0.02 ± 0.01 (P<0.01). CDA-II could significantly down-regulate the expression of DNMTs in MUTZ-1 cells in a dose-(r=0.999, 0.992, 0.995, P<0.01) and time-dependent (r=0.989, 0.981, 0.985, P<0.05) manner, which led to the demethylation of PTEN. Among them, DNMT1 was the most downregulated (F=21.256, P<0.05).

Conclusion: PTEN gene was hypermethylated in high-risk MDS, and target therapy of PTEN demethylation might be a new strategy for MDS therapy. CDA-II could down regulate the expression of DNMTs and lead to PTEN demethylation which induce MUTZ-1 cells apoptosis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Line
  • DNA (Cytosine-5-)-Methyltransferases / genetics
  • DNA (Cytosine-5-)-Methyltransferases / metabolism
  • DNA Methylation / drug effects*
  • DNA Methyltransferase 3B
  • Humans
  • Leukemia, Myeloid, Acute / genetics
  • Leukemia, Myeloid, Acute / metabolism*
  • Myelodysplastic Syndromes / genetics
  • Myelodysplastic Syndromes / metabolism*
  • PTEN Phosphohydrolase / genetics
  • PTEN Phosphohydrolase / metabolism*
  • Peptides / pharmacology*
  • Phenylacetates / pharmacology*

Substances

  • Peptides
  • Phenylacetates
  • cell differentiation agent II
  • DNA (Cytosine-5-)-Methyltransferases
  • PTEN Phosphohydrolase
  • PTEN protein, human