ArticleWorld journal of gastroenterology2006
Identification of specific genes and pathways involved in NSAIDs-induced apoptosis of human colon cancer cells.
Article in World journal of gastroenterology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 22 citations in OpenAlex.
- Tolfenamic acid-induced alterations in genes and pathways in pancreatic cancer cells.Oncotarget · 2017Article
- NSAIDs may regulate EGR-1-mediated induction of reactive oxygen species and non-steroidal anti-inflammatory drug-induced gene (NAG)-1 to initiate intrinsic pathway of apoptosis for the chemoprevention of colorectal cancer.Molecular and cellular biochemistry · 2013Article
- Medullary thyroid cancer--current treatment strategy, novel therapies and perspectives for the future.Hormones & cancer · 2012Review
- Apoptosis of human cholangiocarcinoma cells induced by ESC-3 from Crocodylus siamensis bile.World journal of gastroenterology · 2012Article
- Galangin induces apoptosis of hepatocellular carcinoma cells via the mitochondrial pathway.World journal of gastroenterology · 2010Article
- Effect of 5-LOX/COX-2 common inhibitor DHDMBF30 on pancreatic cancer cell Capan2.World journal of gastroenterology · 2008Article
- Global tumor RNA expression in early establishment of experimental tumor growth and related angiogenesis following COX-inhibition evaluated by microarray analysis.Cancer informatics · 2007Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo study whether indomethacin (IND), a nonselective cyclooxygenase (COX) inhibitor or NS-398 (NS), a COX-2-selective inhibitor, induces apoptosis in human colon cancer cells and which apoptosis-related genes and pathways are involved.
methodsHuman colon cancer Caco-2 cells were treated with either: placebo, IND (0.05-0.5 mmol/L) or NS (0.01-0.2 mmol/L) for 1, 5 and 18 h. We then studied: (1) Cell death by the TUNEL method, (2) mRNA expression of 96 apoptosis-related genes using DNA microarray, (3) expression of selected apoptosis related proteins by Western blotting.
resultsBoth IND and NS induced apoptosis in 30%-50% of Caco-2 cells in a dose dependent manner. IND (0.1 mmol/L for 1 h) significantly up-regulated pro-apoptotic genes in four families: (1) TNF receptor and ligand, (2) Caspase, (3) Bcl-2 and (4) Caspase recruiting domain. NS treatment up-regulated similar pro-apoptotic genes as IND. In addition, IND also down-regulated anti-apoptotic genes of the IAP family.
conclusion(1) Both non-selective and COX-2-selective NSAIDs induce apoptosis in colon cancer cells in a dose dependent manner. (2) Both NSAIDs induce apoptosis by activating two main apoptotic pathways: the death receptor pathway (involving TNF-R) and the mitochondrial pathway. (3) IND induces apoptosis by up-regulating pro-apoptotic genes and down-regulating anti-apoptotic genes, while NS only up-regulates pro-apoptotic genes. (4) Induction of apoptosis in colon cancer cells by NSAIDs may explain in part, their inhibitory action on colon cancer growth.
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