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Electroporation and carrier DNA cause p53 activation, cell cycle arrest, and apoptosis

Dina Lepik1, Viljar Jaks, Lilian Kadaja

  • 1Department of Cell Biology, Institute of Molecular and Cell Biology, Tartu University, 23 Riia Street, Tartu 51010, Estonia. dlepik@ebc.ee

Insights

Electroporation causes cell cycle arrest and apoptosis, affecting p53 protein stability and activity. Polyethylenimine, a transfection agent, did not impact p53 or cellular response.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biotechnology

Background:

  • Transient transfection methods can alter cellular signaling pathways, potentially leading to inaccurate experimental results.
  • The p53 protein plays a critical role in cellular responses to genotoxic stress, mediating apoptosis or growth arrest.

Purpose of the Study:

  • To investigate the impact of electroporation and carrier DNA on the stability, cellular localization, and transcriptional activity of the p53 protein.
  • To compare the cellular effects of electroporation with those of polyethylenimine, another common transfection agent.

Main Methods:

  • Cells were subjected to electroporation and transfection with carrier DNA.
  • The stability, cellular localization, and transcriptional activity of p53 were analyzed.
  • Cellular responses, including cell-cycle arrest and apoptosis, were assessed.
  • The effects of polyethylenimine on p53 and cellular responses were also evaluated.

Main Results:

  • Electroporation induced both p53-dependent and p53-independent cell-cycle arrest and apoptosis.
  • Carrier DNA did not significantly alter these effects.
  • Polyethylenimine did not lead to p53 upregulation or any observable cellular response.

Conclusions:

  • Electroporation is a potent method that can trigger significant cellular responses, including apoptosis and cell-cycle arrest, independent of p53 in some cases.
  • The choice of transfection method is critical, as electroporation significantly impacts cellular pathways, while polyethylenimine appears to have a minimal effect on p53-mediated responses.

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