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Antisense oligodeoxyribonucleotides suppress hematologic cell growth through stepwise release of deoxyribonucleotides

J L Vaerman1, P Moureau, F Deldime

  • 1Laboratoire de Biologie Moleculaire Hématologique, Cliniques St Luc, Université Catholique de Louvain, Clos Chapelle-aux-champs, Brussels, Belgium.

Blood
|July 1, 1997
PubMed

Insights

Antisense oligodeoxyribonucleotides (ODNs) show antiproliferative effects on leukemia cells due to toxic hydrolysis products, not antisense activity. The 3' sequence and d-NMP composition determine toxicity, revealing a non-antisense mechanism.

Area of Science:

  • Molecular Biology
  • Pharmacology
  • Hematology

Background:

  • Antisense oligodeoxyribonucleotides (ODNs) are investigated for cancer therapy by targeting genes involved in cell proliferation.
  • Non-antisense cytotoxic effects of ODNs are increasingly recognized, necessitating re-evaluation of their mechanisms of action.
  • Chronic myeloid leukemia (CML) research utilizes anti-BCR/ABL antisense strategies, making ODN effects on leukemic cells critical.

Purpose of the Study:

  • To re-examine the antiproliferative effects of phosphodiester and phosphorothioate ODNs on leukemic and bone marrow cells.
  • To elucidate the mechanism behind the observed antiproliferative activity, distinguishing between antisense and non-antisense effects.
  • To identify factors influencing ODN-induced cytotoxicity, specifically the role of 3' sequences and hydrolysis products.

Main Methods:

  • Tested phosphodiester and phosphorothioate ODNs on BV173 leukemic cell line and CD34+ bone marrow cells in liquid culture.
  • Varied ODN concentrations and sequences, focusing on the 3' terminal positions.
  • Analyzed the hydrolysis products of ODNs (5' monophosphate deoxyribonucleosides - d-NMPs) and their cytotoxic effects.

Main Results:

  • All tested ODNs showed antiproliferative activity at specific concentrations, except those with cytosine at the two 3' terminal positions.
  • The antiproliferative effect was attributed to the toxicity of d-NMPs, enzymatic hydrolysis products of ODNs.
  • d-NMP toxicity depended on their type (d-CMP non-cytotoxic), concentration, and the presence of other d-NMPs (d-CMP neutralized toxicity).

Conclusions:

  • The antiproliferative activity of ODNs is primarily a non-antisense effect mediated by toxic d-NMPs generated during hydrolysis.
  • ODN efficacy is restricted to conditions favoring d-NMP generation with low d-CMP levels.
  • These findings highlight the importance of considering non-antisense mechanisms, particularly d-NMP toxicity, in ODN-based research and therapy.

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