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Aspirin induces cell death and caspase-dependent phosphatidylserine externalization in HT-29 human colon adenocarcinoma cells
Authors
AA Beg
AW Boddie
+51 more
B Bellosillo
B Bonnotte
B Hoffman
BG Heerdt
CJ Barnes
CY Wang
DJ Elder
DJ Elder
DJ Van Antwerp
DJE Elder
DM Vanags
E Castaño
E Kopp
EK Han
F Oberhammer
GA Piazza
GA Piazza
GM Cohen
JA Efstathiou
JM Zapata
JR Vane
L Qiao
M Tsujii
M Tsujii
M Van Engeland
M Woo
MJ Yin
N Arber
P Ricchi
P Schwenger
PA Hall
PJ Pasricha
R Mangiarotti
R Subbegowda
RA Gupta
RC Duke
RG Shao
RU Janicke
SJ Martin
SJ Shiff
SJ Shiff
SJ Shiff
SK Boolbol
T Mosmann
UK Laemmli
V Cryns
WE Smalley
WL Smith
X Lu
YA Hannun
ZG Liu
Publication date
29 January 2020
Publisher
Nature Publishing Group
Doi
View
on
PubMed
Abstract
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. © 1999 Cancer Research Campaig
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oai:diposit.ub.edu:2445/148832
Last time updated on 14/02/2020
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Last time updated on 11/12/2019