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

Castaño, Esther; Dalmau, Mireia; Barragán, Montserrat; Pueyo, Gloria; Bartrons, Ramón; Gil, J

doi:10.1038/sj.bjc.6990690

Cited by 5 publications

(7 citation statements)

References 22 publications

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“…Cell viability was determined by analyzing phosphatidylserine exposure and membrane integrity by double staining with annexin V‐FITC and PI, prior to flow cytometric analysis (FACSCalibur, Becton Dickinson, Mountain View, CA, USA), as previously described [4]. Data analysis was performed with CellQuest software (Becton Dickinson).…”

Section: Methodsmentioning

confidence: 99%

“…Aspirin and other non‐steroidal anti‐inflammatory drugs (NSAIDs) induce apoptosis in several cell types, including human colorectal tumor cell lines [1–4], fibroblasts [5,6], B‐cell chronic lymphocytic leukemia cells [7] and myeloid leukemia cell lines [8]. Furthermore, administration of NSAIDs induces apoptosis of colon cancer cells in vivo [9,10].…”

Section: Introductionmentioning

confidence: 99%

“…The apoptotic action of NSAIDs was inhibited by the caspase inhibitor Z‐VAD·fmk, demonstrating the involvement of caspases [4,7,8]. However, the pathway leading to caspase activation remains unknown.…”

Section: Introductionmentioning

confidence: 99%

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Aspirin induces apoptosis through mitochondrial cytochrome c release

et al. 2000

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Aspirin and other non-steroidal anti-inflammatory drugs induce apoptosis in many cell types. Although the involvement of caspases has been demonstrated, the mechanism leading to caspase activation remains unknown. We have studied the role of the mitochondrial pathway in aspirin-induced apoptosis. The apoptotic effect of aspirin was analyzed in different cell lines (Jurkat, MOLT-4, Raji and HL-60) showing induction of mitochondrial cytochrome c release and caspases 9, 3 and 8 processing. Furthermore, early aspirin-induced cytochrome c release was not affected by the caspase inhibitor Z-VADW Wfmk and preceded loss of mitochondrial membrane potential. Therefore, aspirin-induced apoptosis involves caspase activation through cytochrome c release. ß

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Aspirin induces apoptosis through mitochondrial cytochrome c release

et al. 2000

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“…NSAIDs inhibit the proliferation of cancer cells by various mechanisms 19–22 . Mechanisms of anticancer activity by NSAIDS include cell cycle arrest and induction of apoptosis or necrosis 17,23 . However, the molecular mechanisms underlying anticancer activities of NSAIDs are very complex, and manifest differentially depending on the cell type 17,24 .…”

Section: Discussionmentioning

confidence: 99%

Apoptotic Effect of Celecoxib Dependent Upon p53 Status in Human Ovarian Cancer Cells

Song

Kim

Juhnn

et al. 2007

Annals of the New York Academy of Sciences

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Celecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor, induces the apoptosis in various cancers in COX-2 dependent and/or independent manners. The p53 protein is mutated in 50% of all human tumors and plays a key role in apoptosis, cell cycle, and the expression of several proteins. In ovarian cancer, the rate of p53 mutation has been shown to be very high and associated with poor prognosis. To explore the importance of functional status of p53 in apoptosis by celecoxib in ovarian cancer cells, the cellular response to celecoxib was determined in SK-OV3 ovarian cancer cells with null type p53 and PA-1 with wild-type p53. Our results showed that celecoxib inhibited cell growth more in PA-1 than in SK-OV3. The underlying antiproliferative mechanism may differ between these two cell types dependent upon the functional status of p53, which plays integral roles in regulating cell cycle and survival. Higher sub-G1 was shown in PA-1 than in SK-OV3 in response to celecoxib (PA-1 versus SK-OV3; 60.28% versus 6.69%). Caspase -8, -9, and -3 were activated in PA-1 cells, but not in SK-OV3 cells. These results suggest that death receptor and mitochondria-mediated apoptotic pathways may be involved in celecoxib-induced apoptosis dependent upon the functional status of p53. Our article demonstrated that the celecoxib effectively inhibited cell growth and induced apoptosis in human ovarian cancer cells with wild-type p53. Thus, apoptotic effect by celecoxib seemed to be different dependent upon the functional status of p53.

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“…As our understanding of apoptosis and its relationship with aging and disease grows, more research should focus on how to prevent functional decline caused by its dysregulation. Several classes of drugs are being studied in relation to apoptosis 58–79 . Enalapril is a drug that has been shown to prevent apoptosis in myocardial cells.…”

Section: The Aging Human Bodymentioning

confidence: 99%

Functional Decline in Aging and Disease: A Role for Apoptosis

Joaquin

Gollapudi

2001

J American Geriatrics Society

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The process of aging and senescence is associated with a decline in several organ functions and ultimately takes away independence and reduces quality of life. The precariously marginal functional reserves of the immune, pulmonary, and cardiovascular systems are among the most important causes of increased hospitalization in the older population. When complicated by chronic diseases, as is often the case, the problem is magnified. Apoptosis, or programmed cell death, is a process that goes on continuously throughout life. It is involved in embryogenesis for proper organ and tissue development. After birth and through adulthood, it helps eliminate unneeded and damaged cells. There is evidence that advanced age is associated with dysregulation of apoptosis. Several studies have shown age-related changes in the levels of proteins and factors that regulate apoptosis. This could explain the age-associated increased prevalence of cancers, certain autoimmune diseases, and neurodegenerative disorders in older people. More studies are needed to further elucidate the process of apoptosis. With this knowledge, the use of gene therapy and apoptosis modulators may someday have therapeutic value in preventing the functional decline we see in the older population.

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

Cited by 5 publications

References 22 publications

Aspirin induces apoptosis through mitochondrial cytochrome c release

Aspirin induces apoptosis through mitochondrial cytochrome c release

Apoptotic Effect of Celecoxib Dependent Upon p53 Status in Human Ovarian Cancer Cells

Functional Decline in Aging and Disease: A Role for Apoptosis

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