Aspirin induces cell death and caspase-dependent phosphatidylserine externalization in HT-29 human colon adenocarcinoma cells.
The induction of cell death by aspirin was analysed in HT-29 colon carcinoma cells. Aspirin induced two hallmarks of apoptosis: nuclear chromatin condensation and increase in phosphatidylserine externalization. However, aspirin did not induce either oligonucleosomal fragmentation of DNA, decrease in DNA content or nuclear fragmentation. The effect of aspirin on Annexin V binding was inhibited by the caspase inhibitor Z-VAD.fmk, indicating the involvement of caspases in the apoptotic action of aspirin. However, aspirin did not induce proteolysis of PARP, suggesting that aspirin does not increase nuclear caspase 3-like activity in HT-29 cells. This finding may be related with the 'atypical' features of aspirin-induced apoptosis in HT-29 cells.
Castaño
E
E
Unitat de Bioquímica, Departament de Ciències Fisiològiques II, Universitat de Barcelona, L'Hospitalet, Spain.
Dalmau
M
M
Barragán
M
M
Pueyo
G
G
Bartrons
R
R
Gil
J
J
D017209:Apoptosis / Q000187:drug effects*; D001241:Aspirin / Q000494:pharmacology*; D015153:Blotting, Western; D020169:Caspases / Q000378:metabolism*; D053938:DNA Fragmentation; D004789:Enzyme Activation / Q000187:drug effects; D019073:HT29 Cells / Q000187:drug effects; D006801:Humans; D010718:Phosphatidylserines / Q000378:metabolism; D011065:Poly(ADP-ribose) Polymerases / Q000378:metabolism
D010718:Phosphatidylserines; D011065:Poly(ADP-ribose) Polymerases; D020169:Caspases; D001241:Aspirin