ArticleMolecular cancer research : MCR2010
NSAID inhibition of prostate cancer cell migration is mediated by Nag-1 Induction via the p38 MAPK-p75(NTR) pathway.
Article in Molecular cancer research : MCR, 2010. 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, 55 citations in OpenAlex.
- Article
- The relationship between nonsteroidal anti-inflammatory drugs and cancer incidence: An umbrella review.Heliyon · 2024Review
- Review
- N-glycosylation of GDF15 abolishes its inhibitory effect on EGFR in AR inhibitor-resistant prostate cancer cells.Cell death & disease · 2022Article
- NSAIDs and Cancer Resolution: New Paradigms beyond Cyclooxygenase.International journal of molecular sciences · 2022Review
- Indolethylamine-N-Methyltransferase Inhibits Proliferation and Promotes Apoptosis of Human Prostate Cancer Cells: A Mechanistic Exploration.Frontiers in cell and developmental biology · 2022Article
- Continuous flow asymmetric synthesis of chiral active pharmaceutical ingredients and their advanced intermediates.Green chemistry : an international journal and green chemistry resource : GC · 2021Review
- Flow Biocatalysis: A Challenging Alternative for the Synthesis of APIs and Natural Compounds.International journal of molecular sciences · 2021Review
- Grape Seed Proanthocyanidins Induce Apoptosis and Cell Cycle Arrest of HepG2 Cells Accompanied by Induction of the MAPK Pathway and NAG-1.Antioxidants (Basel, Switzerland) · 2020Article
- Serum amyloid A inhibits astrocyte migration via activating p38 MAPK.Journal of neuroinflammation · 2020Article
- Effects of non-steroidal anti-inflammatory drug-activated gene-1 on Ganoderma lucidum polysaccharides-induced apoptosis of human prostate cancer PC-3 cells.International journal of oncology · 2018Article
- Therapeutic Effect of Repurposed Temsirolimus in Lung Adenocarcinoma Model.Frontiers in pharmacology · 2018Article
- The ethanol extracts of sporoderm-broken spores of Ganoderma lucidum inhibit colorectal cancer in vitro and in vivo.Oncology reports · 2017Article
- p75NTR promotes survival of breast cancer resistant cells by regulating Bcl-2/Bax and MAPK pathway.International journal of clinical and experimental pathology · 2017Article
- Prostate Cancer and Aspirin Use: Synopsis of the Proposed Molecular Mechanisms.Frontiers in pharmacology · 2017Review
- Article
- Evasion of anti-growth signaling: A key step in tumorigenesis and potential target for treatment and prophylaxis by natural compounds.Seminars in cancer biology · 2015Review
- High enantioselective Novozym 435-catalyzed esterification of (R,S)-flurbiprofen monitored with a chiral stationary phase.Applied biochemistry and biotechnology · 2015Article
- Reduced expression of GDF-15 is associated with atrophic inflammatory lesions of the prostate.The Prostate · 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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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The nonsteroidal anti-inflammatory drugs (NSAID) R-flurbiprofen and ibuprofen have been shown to induce expression of p75(NTR) (neurotrophin receptor) in prostate cancer cell lines. p75(NTR), a tumor necrosis factor receptor superfamily member, is a proapoptotic protein that functions as a tumor suppressor in the human prostate. Expression of p75(NTR) is lost as prostate cancer progresses and is minimal in several metastatic prostate cancer cell lines. NSAIDs induce p75(NTR) through activation of the p38 mitogen-activated protein kinase (MAPK) pathway, with a concomitant decrease in cell survival. Here, we show that treatment with R-flurbiprofen and ibuprofen induces expression of the NSAID-activated gene-1 (Nag-1) protein, a divergent member of the TGF beta (TGF-β) family, in PC-3 cells. Using the selective pharmacologic inhibitor of p38 MAPK, SB202190, and p38 MAPK-specific siRNA (small interfering RNA), we show that Nag-1 induction following NSAID treatment is mediated by the p38 MAPK pathway. p75(NTR)-specific siRNA pretreatment shows that Nag-1 induction by NSAIDs is downstream of p75(NTR) induction. Decreased survival of NSAID-treated cells is rescued by p75(NTR)-specific siRNA but not by Nag-1 siRNA. Transwell chamber and in vitro wound healing assays demonstrate decreased cell migration upon NSAID treatment. Pretreatment of PC-3 cells with p75(NTR) and Nag-1-specific siRNA shows that NSAID inhibition of cell migration is mediated by Nag-1 and p75(NTR). These results demonstrate a role for Nag-1 in NSAID inhibition of cell migration, but not survival.
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