We previously demonstrated that the cytotoxicity associated with exposure o
f HCT116 cells to deoxycholic acid was due to the induction of apoptosis. H
ere we show that this results in activation of caspase 3 and that over expr
ession of bcl-2 can suppress this. Surprisingly, inhibition of apoptosis by
over expression of bcl-2 or incubation with calphostin C, a PKC inhibitor,
did not enhance cell survival, but instead caused a switchover to death by
necrosis. Hence, DCA-induced apoptosis requires caspase activity and both
bcl-2 and PKC can determine the type of cell death induced by deoxycholic a
cid. (C) 2000 Elsevier Science Ireland Ltd, All rights reserved.