ArticleCancer cell international2013
Overexpression of p65 attenuates celecoxib-induced cell death in MDA-MB-231 human breast cancer cell line.
Article in Cancer cell international, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- ROR activation by Nobiletin enhances antitumor efficacy via suppression of IκB/NF-κB signaling in triple-negative breast cancer.Cell death & disease · 2022Article
- Ampelopsin Suppresses Stem Cell Properties Accompanied by Attenuation of Oxidative Phosphorylation in Chemo- and Radio-Resistant MDA-MB-231 Breast Cancer Cells.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Disabling the Nuclear Translocalization of RelA/NF-κB by a Small Molecule Inhibits Triple-Negative Breast Cancer Growth.Breast cancer (Dove Medical Press) · 2021Article
- Celecoxib enhances sensitivity to chemotherapy drugs of T-cell lymphoma.Oncology letters · 2018Article
- Curcumol potentiates celecoxib-induced growth inhibition and apoptosis in human non-small cell lung cancer.Oncotarget · 2017Article
- Neuroprotective Role of Exogenous Brain-Derived Neurotrophic Factor in Hypoxia-Hypoglycemia-Induced Hippocampal Neuron Injury via Regulating Trkb/MiR134 Signaling.Journal of molecular neuroscience : MN · 2017Article
- The lipoxin ANaunyn-Schmiedeberg's archives of pharmacology · 2017Article
- Protein Kinase R Mediates the Inflammatory Response Induced by Hyperosmotic Stress.Molecular and cellular biology · 2017Article
- Roles of coinhibitory molecules B7-H3 and B7-H4 in esophageal squamous cell carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Celecoxib and fish oil: a combination strategy for decreased inflammatory mediators in early stages of experimental mammary cancer.Inflammopharmacology · 2016Article
- Targeting the NFκB signaling pathways for breast cancer prevention and therapy.Current medicinal chemistry · 2015Review
- Sensitization of U937 leukemia cells to doxorubicin by the MG132 proteasome inhibitor induces an increase in apoptosis by suppressing NF-kappa B and mitochondrial membrane potential loss.Cancer cell international · 2014Article
- B7-H3 is overexpressed in patients suffering osteosarcoma and associated with tumor aggressiveness and metastasis.PloS one · 2013Article
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Authors and funding
5 authors.
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Abstract
backgroundCelecoxib is a selective cyclooxygenase (COX)-2 inhibitor that has been reported to reduce the risk of breast cancer. In our previous study, celecoxib induced apoptosis and caused cell cycle arrest at the G0/G1 phase in the breast cancer cell line MDA-MB-231, and its effects were mediated by downregulation of NF-κB signaling. The NF-κB p65/RelA subunit may play a role in cell death through the activation of anti-apoptotic target genes including the inhibitor of apoptosis (IAP) and Bcl-2 families, and inhibition of protein kinase B/Akt. The aim of the present study was to investigate p65 as the potential target of celecoxib treatment and determine whether p65 overexpression can override the inhibitory effect of celecoxib on NF-κB activity and affect cell survival.
methodsThe effects of p65 overexpression on celecoxib-inhibited NF-κB transcriptional activity were examined by western blotting, electrophoretic mobility shift assay (EMSA) and luciferase reporter gene assay. Cell viability and cell death were evaluated by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide (MTT) assay, and the levels of cleaved poly(ADP-ribose) polymerase (PARP) and caspase. Anti-apoptotic NF-κB target genes and cell cycle regulators were examined by western blotting to screen for the expression of target genes under direct regulation by p65.
resultsOverexpression of p65 increased NF-κB transcriptional activity and interfered with celecoxib-mediated apoptosis as assessed by MTT assay and caspase-3, caspase-9, and PARP expressions. Exogenously overexpressed p65 upregulated NF-κB-responsive genes, including anti-apoptotic genes such as survivin and XIAP, and the cell cycle regulatory gene cyclin D1. However, p65 overexpression did not affect celecoxib-induced p-Akt inactivation, suggesting that celecoxib might have separate molecular mechanisms for regulating Akt signaling independently of its inhibition of NF-κB transcriptional activity.
conclusionsp65 is a pivotal anti-apoptotic factor that can reverse celecoxib-induced growth inhibition in MDA-MB-231 cells.
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