Aspirin induces cell death and caspase-dependent phosphatidylserine externalization in HT-29 human colon adenocarcinoma cells

• Published in: British Journal of Cancer Vol. 81; no. 2; pp. 294 - 299
• Main Authors: CASTANO, E, DALMAU, M, BARRAGAN, M, PUEYO, G, BARTRONS, R, GIL, J
• Format: Journal Article
• Language: English
• Published: Basingstoke Nature Publishing Group 01.09.1999; Cancer Research UK
• Subjects: Antineoplastic agents; Apoptosi; Apoptosis; Apoptosis - drug effects; Aspirin; Aspirin - pharmacology; Aspirina; Biological and medical sciences; Blotting, Western; Caspases - metabolism; DNA Fragmentation; Drug side effects; Efectes secundaris dels medicaments; Enzyme Activation - drug effects; Farmacologia; General aspects; HT29 Cells - drug effects; Humans; Medical sciences; Pharmacology; Pharmacology. Drug treatments; Phosphatidylserines - metabolism; Poly(ADP-ribose) Polymerases - metabolism; Regular; Adenocarcinoma; Antineoplastic agent; Human; Enzyme; Cysteine endopeptidases; Cytotoxicity; Malignant tumor; Acetylsalicylic acid; In vitro; Colonic disease; Non steroidal antiinflammatory agent; Peptidases; Interleukin 1-β converting enzyme; Cell death; Established cell line; Digestive diseases; Hydrolases; Intestinal disease; Colon; Salicylates; Mechanism of action; Phosphatidylserine; Apoptosis
• ISSN: 0007-0920; 1476-5381; 1532-1827
• DOI: 10.1038/sj.bjc.6690690

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.