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- W2507344155 abstract "Previous experiments have demonstrated that double-stranded RNAs (dsRNAs) can exert an antiprolif- erative effect on human tumor cells, independent of interferon (IFN) induction. However, the mechanism by which dsRNAs inhibit tumor growth has not been elucidated. As a flrst step in determining the molecular events responsible for growth ar- rest, we have explored the role of signal transduction through the cAMP system in the antiproliferative effect of the mis- induced antiproliferative effect. Measurement of adenylate cyclase activation showed a dose-dependent increase in activity at antiproliferative mismatched dsRNA concentrations, but not at lower, nonantiproliferative doses. This increase in activity was rapid, seen as early as 30 sec after initiation of treatment, and it was sustained at peak levels for 1-2 hr. Analysis of the intracellular cAMP concentration gave similar kinetics of induction. Exposure of cells to the stable cAMP analogue dibutyryl cAMP yielded dose-dependent inhibition of cell growth. The cAMP phosphodiesterase inhibitor 3-isobutyl-1- methylxanthine also inhibited proliferation. In contrast, nei- ther H-7 nor HA1004 had an effect on growth inhibition induced by human natural IFN-a treatment. In addition, antiproliferative doses of IFN-a did not increase cAMP con- centrations. These results indicate that the cAMP system is utilized by mismatched dsRNA as an early signal transduction mechanism for growth control. Furthermore, the antiprolifer- ative effects induced by mismatched dsRNA and IFN can occur by different mechanisms of action." @default.
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- W2507344155 date "2016-01-01" @default.
- W2507344155 modified "2023-09-27" @default.
- W2507344155 title "Cyclic AMP mediates the direct antiproliferative action of" @default.
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