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Phosphodiester oligonucleotides inhibit mitosis and trigger apoptosis by a non-antisense, p53-mediated mechanism

Laura Papucci1, Nicola Schiavone, Martino Donnini

  • 1Department of Experimental Pathology and Oncology, University of Florence, Italy. lpapucci@yahoo.com

Antisense & Nucleic Acid Drug Development
|May 23, 2002
PubMed

Insights

Oligodeoxyribonucleotides (ODNs) can inhibit cell division and induce cell death through a non-antisense mechanism. This process involves the p53 protein and is triggered by the free ends of the DNA molecules.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • Oligodeoxyribonucleotides (ODNs) are used for gene silencing in labs.
  • ODNs can cause unintended non-antisense effects.
  • Previous studies showed double-stranded DNA oligonucleotides activate p53.

Purpose of the Study:

  • To investigate the non-antisense effects of phosphorodiester ODNs in cultured cells.
  • To determine the mechanism behind ODN-induced mitosis inhibition and apoptosis.
  • To explore the role of p53 and ODN structure in these effects.

Main Methods:

  • Lipotransfection of cultured cells with phosphorodiester ODNs (30-mers).
  • Assessment of mitosis inhibition and apoptosis induction.
  • Evaluation of the requirement for wild-type p53 protein.
  • Analysis of ODN concentration and free end dependency.

Main Results:

  • Lipotransfection with ODNs induced mitosis inhibition and apoptosis.
  • These effects were mediated by a non-antisense mechanism requiring wild-type p53.
  • The effects were dependent on ODN concentration and the 3' and 5' free ends of the ODNs.
  • p53 activation was independent of the ODN sequence.

Conclusions:

  • Phosphorodiester ODNs can induce cell death via a p53-dependent, non-antisense pathway.
  • The free ends of ODNs are crucial for activating p53, mimicking DNA damage responses.
  • This mechanism offers a new perspective on ODN activity beyond gene silencing.

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