ArticleMolecular and cellular biochemistry2011
Inhibitory effect of celecoxib in lung carcinoma by regulation of cyclooxygenase-2/cytosolic phospholipase A₂ and peroxisome proliferator-activated receptor gamma.
Article in Molecular and cellular biochemistry, 2011. 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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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.
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Who cites it
7 citing papers in PubMed, 20 citations in OpenAlex.
- Preparation, COX-2 Inhibition and Anticancer Activity of Sclerotiorin Derivatives.Marine drugs · 2020Article
- Highly bioavailable Berberine formulation improves Glucocorticoid Receptor-mediated Insulin ResistanceInternational journal of biological sciences · 2020Article
- The Effect of Biotinylated PAMAM G3 Dendrimers Conjugated with COX-2 Inhibitor (celecoxib) and PPARγ Agonist (Fmoc-L-Leucine) on Human Normal Fibroblasts, Immortalized Keratinocytes and Glioma Cells in Vitro.Molecules (Basel, Switzerland) · 2019Article
- Chemotherapy induces ovarian cancer cell repopulation through the caspase 3-mediated arachidonic acid metabolic pathway.OncoTargets and therapy · 2017Article
- [Interaction of anesthetics and analgesics with tumor cells].Der Anaesthesist · 2014Review
- Induction but not inhibition of COX-2 confers human lung cancer cell apoptosis by celecoxib.Journal of lipid research · 2013Article
- Celecoxib induces apoptosis and cell-cycle arrest in nasopharyngeal carcinoma cell lines via inhibition of STAT3 phosphorylation.Acta pharmacologica Sinica · 2012Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Celecoxib is a potent nonsteroid anti-inflammatory drug (NSAID) that has demonstrated great promise in cancer chemoprevention and treatment. The goal of this study was to determine the inhibitory effect and mechanism of celecoxib on Lewis lung carcinoma. The effect of celecoxib on viability of Lewis lung carcinoma cells was assessed with methyl thiazolyl tetrazolium (MTT) assay. Apoptosis and the mitochondrial membrane potential were detected by flow cytometric assay. The protein expression of cytosolic phospholipase A(2) (cPLA(2)), cyclooxygenase-2 (COX-2), and peroxisome proliferator-activated receptor gamma (PPARγ) were determined by Western blot analysis. The concentrations of arachidonic acid (AA) and prostaglandin E(2) (PGE(2)) in culture supernatants were measured by the methods of RP-HPLC and PGE(2)-specific ELISA, respectively. Celecoxib inhibited the proliferation of Lewis lung carcinoma and induced apoptosis in a dose-dependent manner by breakdown of mitochondrial membrane potential. The protein expressions of cPLA(2) and PPARγ were upregulated, but COX-2 protein expression was downregulated in the Lewis lung carcinoma cells exposed to celecoxib. The amount of AA was increased and PGE(2) was decreased in the culture supernatant, respectively. The ratio of AA to PGE(2) was increased in a dose-dependent manner. The major findings in this study are that celecoxib could inhibit the viability of Lewis lung carcinoma cells by interference of the AA pathway and upregulation of PPARγ simultaneously, which are novel and important since the molecular mechanisms of celecoxib underlying the anti-neoplastic effects remain unclear.
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