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Effect of cell cycle growth arrest on global DNA methylation status in human lung epithelial-like (A549) cells

Mihalis I Panayiotidis1, Ray C Rancourt, Aglaia Pappa

  • 1Department of Pediatrics, National Jewish Medical and Research Center, Denver, CO 80206, USA. panagiotidism@unc.edu

In Vivo (Athens, Greece)
|January 6, 2007
PubMed
Abstract

Insights

Global DNA methylation in A549 cells is not primarily driven by hyperoxia-induced cell cycle arrest. This study investigated cell cycle arrest and DNA methylation changes in A549 cells under hyperoxia.

Area of Science:

  • Cell Biology
  • Epigenetics
  • Cancer Research

Background:

  • Prolonged hyperoxia exposure decreases global DNA methylation in A549 cells.
  • Hyperoxia also induces cell growth arrest in these cells.

Purpose of the Study:

  • To investigate if global DNA methylation changes are a consequence of hyperoxia-induced cell cycle growth arrest.
  • To determine the relationship between cell cycle phase and DNA methylation status.

Main Methods:

  • A549 cells were growth arrested using resveratrol (S-phase) or colcemid (G2/M-phase).
  • Cells were exposed to normoxia or hyperoxia for varying durations (1-5 days) to study hyperoxia-induced growth arrest kinetics.
  • Global DNA methylation status was assessed in synchronized and hyperoxia-exposed cells.

Main Results:

  • Hyperoxia induced G2/M growth arrest from day 2 onwards.
  • Resveratrol synchronized 66.5% of cells to S-phase; colcemid synchronized 97% to G2/M-phase.
  • No alterations in global DNA methylation were observed in cells arrested at either S- or G2/M-phase.

Conclusions:

  • Hyperoxia-induced cell cycle growth arrest does not appear to be the primary determinant of global DNA methylation status in A549 cells.
  • The findings suggest that other mechanisms may be responsible for hyperoxia-induced changes in DNA methylation.

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