29 January 2009
Incubation with DNase I inhibits tumor cell proliferationSusana Alcazar-LeyvaADFG, Eduarda CeronBC, Felipe MassoBD, Luis F. MontanoADEF, Patricia GorocicaBC, Noe Alvarado-VasquezABCDEFG
Med Sci Monit 2009; 15(2): CR51-55 :: ID: 869552
Deoxyribonuclease I (DNase-I) plays an important role in the elimination of damaged-, aging- or cancer cells. Various authors suggest that programmed cell death (PCD) is attenuated in cancer cells due to a reduced activity of DNase-I.
Material and Method
In this work, we evaluated cell viability (violet crystal stain), cell proliferation (tritiated thymidine) and DNA degradation of tumoral cells (Calu-1, SK-MES-1, HeLa, HEp-2, L-929) incubated with different concentrations of DNase I. PBMN cells and human fetal fibroblasts served as controls.
Our results showed a >90% decrease in the viability of HeLa and HEp-2 cells, and >50%<90% decline in Calu-1, SK-MES-1 and L-929 cell viability, incubated with 9 mg/ml of DNase-I in comparison with control cells (p<0.05). The incorporation of [3H]thymidine showed a 50% decrease in tumoral cells. Control cells showed no significant differences. Tumor cell DNA degradation was observed after nuclease treatment, however the typical DNA ladder, characteristic of the apoptotic cell, was not observed. The morphology of some DNAse-I treated tumor cells suggested autoschizis
Our results suggest that the use of a DNA nuclease might have some benefits in the treatment of cancer since it inhibits cell growth, probably by inducing autoschizis.
Keywords: Neoplasms - pathology, Deoxyribonuclease I - pharmacology, DNA - analysis, Cell Survival - drug effects, Cell Shape - drug effects, Cell Proliferation - drug effects, Thymidine - metabolism
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