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KMID : 1161520050090040191
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Animal Cells and Systems
2005 Volume.9 No. 4 p.191 ~ p.198
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6-Aminonicotinamide induces G1 arrest by elevating p27kip1 as well as inhibiting cdk2, cyclin E and p-Rb in IMR32 neuroblastoma cell line
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Engliez Souad Ahmad
Park In-Kook
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Abstract
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The effects of 6?aminonicotinamide (6?AN) on viability of IMR32 neuroblastoma cells in the presence of ATP or NAD+ have been investigated. 6?AN caused marked reduction in cell viability and similar observations were also made with cells treated with 6?AN+ATP. However, cells treated with 6?AN+NAD+ showed cell viability similar to untreated cells. Morphologically, 6?AN and 6?AN+ATP treated cells showed loss of neurites, polyhedric shapes, shrinkage of cell bodies and formation of lysed cells, while 6?AN+NAD+ cells did not show any such changes. The flow cytometry analysis demonstrated that 6?AN increased cell population in G0/G1 phase and decreased cell population in S and G2/M phase following a 72 h exposure. Western blot analysis showed that 6?AN stimulated a substantial increase in the level of the cdk inhibitor p27kip1, but lowered the levels of cdk2, cyclin E and p?Rb. However, cdc25A and p53R2 were not significantly affected. Immunofluorscence staining of p27kip1, cdk2, cyclin E and p?Rb revealed close correlation between the signal observed in the Western blot analysis. 6?AN+ATP treated cells showed similar results obtained with 6?AN treated cells in expression of cdk2, cyclin E, p?Rb proteins and p27kip1. 6?AN+NAD+cells showed greater expression of cdk2, cyclin E and p?Rb than those in 6?AN and 6?AN+ATP treated cells. The results suggest that 6?AN induced the G0/G1 phase arrest in IMR32 neuroblastoma cell lines through the increase of p27kip1 and the decrease of cdk2, cyclin E and p?Rb.
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KEYWORD
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6-Aminonicotinamide, IMR32 cells, ATP, NAD+, G1 arrest
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