ReviewCancer metastasis reviews2011
COX inhibitors directly alter gene expression: role in cancer prevention?
Review in Cancer metastasis reviews, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 41 citations in OpenAlex.
- The Sufficient Immunoregulatory Effect of Autologous Bone Marrow-Derived Mesenchymal Stem Cell Transplantation on Regulatory T Cells in Patients with Refractory Rheumatoid Arthritis.Journal of immunology research · 2020Trial
- PIKFYVE inhibitors trigger interleukin-24-dependent cell death of autophagy-dependent melanoma.Molecular oncology · 2024Article
- Role of the Stress- and Inflammation-Induced Cytokine GDF-15 in Cardiovascular Diseases: From Basic Research to Clinical Relevance.Reviews in cardiovascular medicine · 2023Review
- Targeting integrin αvβ3 with indomethacin inhibits patient-derived xenograft tumour growth and recurrence in oesophageal squamous cell carcinoma.Clinical and translational medicine · 2021Article
- Metabolism pathways of arachidonic acids: mechanisms and potential therapeutic targets.Signal transduction and targeted therapy · 2021Review
- NSAIDs-dependent adaption of the mitochondria-proteasome system in immortalized human cardiomyocytes.Scientific reports · 2020Article
- Profiles of histidine-rich glycoprotein associate with age and risk of all-cause mortality.Life science alliance · 2020Article
- Inhibition of cyclooxygenase-2 sensitizes lung cancer cells to radiation-induced apoptosis.Oncology letters · 2017Article
- Effects of celecoxib and ibuprofen on metabolic disorders induced by Walker-256 tumor in rats.Molecular and cellular biochemistry · 2015Article
- NSAIDs inhibit tumorigenesis, but how?Clinical cancer research : an official journal of the American Association for Cancer Research · 2014Review
- The involvement of endoplasmic reticulum stress in the suppression of colorectal tumorigenesis by tolfenamic acid.Cancer prevention research (Philadelphia, Pa.) · 2013Article
- A novel NSAID derivative, phospho-ibuprofen, prevents AOM-induced colon cancer in rats.International journal of oncology · 2013Article
- MT1-MMP expression level status dictates the in vitro action of lupeol on inflammatory biomarkers MMP-9 and COX-2 in medulloblastoma cells.Inflammopharmacology · 2013Article
- Proteasome inhibitor MG132 induces NAG-1/GDF15 expression through the p38 MAPK pathway in glioblastoma cells.Biochemical and biophysical research communications · 2013Article
- NAG-1/GDF15 transgenic mouse has less white adipose tissue and a reduced inflammatory response.Mediators of inflammation · 2013Article
- Phospholipase A2G1B polymorphisms and risk of colorectal neoplasia.International journal of molecular epidemiology and genetics · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Inflammation is an important contributor to the development and progression of human cancers. Inflammatory lipid metabolites, prostaglandins, formed from arachidonic acid by prostaglandin H synthases commonly called cyclooxygenases (COXs) bind to specific receptors that activate signaling pathways driving the development and progression of tumors. Inhibitors of prostaglandin formation, COX inhibitors, or nonsteroidal anti-inflammatory drugs (NSAIDs) are well documented as agents that inhibit tumor growth and with long-term use prevent tumor development. NSAIDs also alter gene expression independent of COX inhibition and these changes in gene expression also appear to contribute to the anti-tumorigenic activity of these drugs. Many NSAIDs, as illustrated by sulindac sulfide, alter gene expressions by altering the expression or phosphorylation status of the transcription factors specificity protein 1 and early growth response-1 with the balance between these two events resulting in increases or decreases in specific target genes. In this review, we have summarized and discussed the various genes altered by this mechanism after NSAID treatment and how these changes in expression relate to the anti-tumorigenic activity. A major focus of the review is on NSAID-activated gene (NAG-1) or growth differentiation factor 15. This unique member of the TGF-β superfamily is highly induced by NSAIDs and numerous drugs and chemicals with anti-tumorigenic activities. Investigations with a transgenic mouse expressing the human NAG-1 suggest it acts to suppress tumor development in several mouse models of cancer. The biochemistry and biology of NAG-1 were discussed as potential contributor to cancer prevention by COX inhibitors.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.