ArticleThe Journal of pharmacology and experimental therapeutics2011
Oxidative stress mediates through apoptosis the anticancer effect of phospho-nonsteroidal anti-inflammatory drugs: implications for the role of oxidative stress in the action of anticancer agents.
Article in The Journal of pharmacology and experimental therapeutics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 50 citations in OpenAlex.
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- Ibuprofen and nimesulide derivatives selectively induce apoptosis in HER2-positive breast cancer via inhibition of the PLA₂-COX-2-NF-κB pathway.Molecular biology reports · 2026Article
- Potential effect of EGCG on the anti-tumor efficacy of metformin in melanoma cells.Journal of Zhejiang University. Science. B · 2021Article
- Medicinal Chemistry Targeting Mitochondria: From New Vehicles and Pharmacophore Groups to Old Drugs with Mitochondrial Activity.International journal of molecular sciences · 2020Review
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- Activation of antioxidant defences of human mammary epithelial cells under leptin depend on neoplastic state.BMC cancer · 2018Article
- 5-Fluorouracil-induced mitochondrial oxidative cytotoxicity and apoptosis are increased in MCF-7 human breast cancer cells by TRPV1 channel activation but not Hypericum perforatum treatment.Molecular and cellular biochemistry · 2018Article
- Anti-allodynic effect of theoesberiven F in a vincristine-induced neuropathy model.Experimental and therapeutic medicine · 2016Article
- TrxR1 as a potent regulator of the Nrf2-Keap1 response system.Antioxidants & redox signaling · 2015Review
- NSAIDs and Colorectal Cancer Control: Promise and Challenges.Current pharmacology reports · 2015Article
- Hitting the Bull's-Eye in Metastatic Cancers-NSAIDs Elevate ROS in Mitochondria, Inducing Malignant Cell Death.Pharmaceuticals (Basel, Switzerland) · 2015Review
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- Phospho-sulindac inhibits pancreatic cancer growth: NFATc1 as a drug resistance candidate.International journal of oncology · 2014Article
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- A novel Ras inhibitor (MDC-1016) reduces human pancreatic tumor growth in mice.Neoplasia (New York, N.Y.) · 2013Article
- Aerosol administration of phospho-sulindac inhibits lung tumorigenesis.Molecular cancer therapeutics · 2013Article
- A novel NSAID derivative, phospho-ibuprofen, prevents AOM-induced colon cancer in rats.International journal of oncology · 2013Article
- New NSAID targets and derivatives for colorectal cancer chemoprevention.Recent results in cancer research. Fortschritte der Krebsforschung. Progres dans les recherches sur le cancer · 2013Review
- Prodrugs of nonsteroidal anti-inflammatory drugs (NSAIDs), more than meets the eye: a critical review.International journal of molecular sciences · 2012Review
- Priming effect of aspirin for tumor cells to augment cytotoxic action of cisplatin against tumor cells: implication of altered constitution of tumor microenvironment, expression of cell cycle, apoptosis, and survival regulatory molecules.Molecular and cellular biochemistry · 2012Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
We assessed the relationship between oxidative stress, cytokinetic parameters, and tumor growth in response to novel phospho-nonsteroidal anti-inflammatory drugs (NSAIDs), agents with significant anticancer effects in preclinical models. Compared with controls, in SW480 colon and MCF-7 breast cancer cells, phospho-sulindac, phospho-aspirin, phospho-flurbiprofen, and phospho-ibuprofen (P-I) increased the levels of reactive oxygen and nitrogen species (RONS) and decreased GSH levels and thioredoxin reductase activity, whereas the conventional chemotherapeutic drugs (CCDs), 5-fluorouracil (5-FU), irinotecan, oxaliplatin, chlorambucil, paclitaxel, and vincristine, did not. In both cell lines, phospho-NSAIDs induced apoptosis and inhibited cell proliferation much more potently than CCDs. We then treated nude mice bearing SW480 xenografts with P-I or 5-FU that had an opposite effect on RONS in vitro. Compared with controls, P-I markedly suppressed xenograft growth, induced apoptosis in the xenografts (8.9 ± 2.7 versus 19.5 ± 3.0), inhibited cell proliferation (52.6 ± 5.58 versus 25.8 ± 7.71), and increased urinary F2-isoprostane levels (10.7 ± 3.3 versus 17.9 ± 2.2 ng/mg creatinine, a marker of oxidative stress); all differences were statistically significant. 5-FU's effects on tumor growth, apoptosis, proliferation, and F2-isoprostane were not statistically significant. F2-isoprostane levels correlated with the induction of apoptosis and the inhibition of cell growth. P-I induced oxidative stress only in the tumors, and its apoptotic effect was restricted to xenografts. Our data show that phospho-NSAIDs act against cancer through a mechanism distinct from that of various CCDs, underscore the critical role of oxidative stress in their effect, and indicate that pathways leading to oxidative stress may be useful targets for anticancer strategies.
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