NOSH-sulindac inhibited cell proliferation, induced apoptosis, and caused G2/M cell cycle block.
NO-ASA inhibited the growth of BxPC-3 cells (IC50 = 13 μM), by inhibiting proliferation modestly and inducing apoptosis, necrosis and G1/S cell cycle block.
VN and VS2 were the two most active compounds against A375 (IC50 of 4.7 and 2.6 μM, respectively), causing apoptosis and cell cycle block.
The analysis of the ploidy of minichromosomes in cells that are released from arrest demonstrates that the sister molecules are properly segregated when the cell cycle block is removed.
Cells were fixed one day after applying the cell cycle block.
No cell cycle block was observed if the treatment with zeocin occurred in G2 phase and the cells divided normally.
The data suggest that caffeine, in the presence of DNA damage, enables partial (30%) overriding of the DNA damage-induced G2 phase cell cycle block.
This could be due to cell cycle block in the G2-M phase or preferential apoptosis of these cells in late S and G2-M.
To this end, U2OS cells were synchronized (double thymidine block, see Materials and methods) and subsequently harvested at different time points after release from this cell cycle block.
Indeed, coexpression of cyclin D1 and cdk4, but not of the cyclin E/cdk2 complex, can reverse a p107-induced cell cycle block [13] [20]).
At 12 hours after release from the cell cycle block (t = 12) the majority of cells was in the G2 and/or M phase.
