ArticleProceedings of the National Academy of Sciences of the United States of America1995
Nonsteroidal antiinflammatory drugs cause apoptosis and induce cyclooxygenases in chicken embryo fibroblasts.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
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Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 209 citations in OpenAlex.
- Interventions for actinic keratoses.The Cochrane database of systematic reviews · 2012Pooled it
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- Synthesis, Molecular Docking and Anticancer Activity of Diflunisal Derivatives as Cyclooxygenase Enzyme Inhibitors.Molecules (Basel, Switzerland) · 2018Article
- Induction but not inhibition of COX-2 confers human lung cancer cell apoptosis by celecoxib.Journal of lipid research · 2013Article
- Synthetic lethal screening with small-molecule inhibitors provides a pathway to rational combination therapies for melanoma.Molecular cancer therapeutics · 2012Article
- Pleiotropic action of AP-1 in v-Src-transformed cells.Journal of virology · 2011Article
- PGE2 receptor EP2 mediates the antagonistic effect of COX-2 on TGF-beta signaling during mammary tumorigenesis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2010Article
- NS-398, ibuprofen, and cyclooxygenase-2 RNA interference produce significantly different gene expression profiles in prostate cancer cells.Molecular cancer therapeutics · 2009Article
- Topical ophthalmic NSAIDs: a discussion with focus on nepafenac ophthalmic suspension.Clinical ophthalmology (Auckland, N.Z.) · 2008Article
- Novel targets and new potential: developments in the treatment of inflammation in chronic kidney disease.Expert opinion on investigational drugs · 2008Review
- Overexpression of the prostaglandin E2 receptor EP2 results in enhanced skin tumor development.Oncogene · 2006Article
- The inhibition of lung colonization of B16-F10 melanoma cells in EFA-deficient animals is related to enhanced apoptosis and reduced angiogenesis.Clinical & experimental metastasis · 2006Article
- Inhibition of human neuroblastoma cell growth by CAY10404, a highly selective Cox-2 inhibitor.Journal of neuro-oncology · 2005Article
- Antimetastatic activity of a cyclooxygenase-2 inhibitor.British journal of cancer · 2004Article
- Nimesulide inhibits proliferation via induction of apoptosis and cell cycle arrest in human gastric adenocarcinoma cell line.World journal of gastroenterology · 2003Article
- Cyclo-oxygenase inhibition reduces tumour growth and metastasis in an orthotopic model of breast cancer.British journal of cancer · 2002Article
- Effect of non-steroidal anti-inflammatory drugs on colon carcinoma Caco-2 cell responsiveness to topoisomerase inhibitor drugs.British journal of cancer · 2002Article
- Disparate effects of non-steroidal anti-inflammatory drugs on apoptosis in guinea-pig gastric mucous cells: inhibition of basal apoptosis by diclofenac.British journal of pharmacology · 2002Article
- Review
- Dehydration activates an NF-kappaB-driven, COX2-dependent survival mechanism in renal medullary interstitial cells.The Journal of clinical investigation · 2000Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Programmed cell death (apoptosis) is an intrinsic part of organismal development and aging. Here we report that many nonsteroidal antiinflammatory drugs (NSAIDs) cause apoptosis when applied to v-src-transformed chicken embryo fibroblasts (CEFs). Cell death was characterized by morphological changes, the induction of tissue transglutaminase, and autodigestion of DNA. Dexamethasone, a repressor of cyclooxygenase (COX) 2, neither induced apoptosis nor altered the NSAID effect. Prostaglandin E2, the primary eicosanoid made by CEFs, also failed to inhibit apoptosis. Expression of the protooncogene bcl-2 is very low in CEFs and is not altered by NSAID treatment. In contrast, p20, a protein that may protect against apoptosis when fibroblasts enter G0 phase, was strongly repressed. The NSAID concentrations used here transiently inhibit COXs. Nevertheless, COX-1 and COX-2 mRNAs and COX-2 protein were induced. In some cell types, then, chronic NSAID treatment may lead to increased, rather than decreased, COX activity and, thus, exacerbate prostaglandin-mediated inflammatory effects. The COX-2 transcript is a partially spliced and nonfunctional form previously described. Thus, these findings suggest that COXs and their products play key roles in preventing apoptosis in CEFs and perhaps other cell types.
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