ArticleCancer biotherapy & radiopharmaceuticals2013
Different cell cycle modulation by celecoxib at different concentrations.
Article in Cancer biotherapy & radiopharmaceuticals, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Diclofenac down-regulates COX-2 induced expression of CD44 and ICAM-1 in human HT29 colorectal cancer cells.Naunyn-Schmiedeberg's archives of pharmacology · 2021Article
- Celecoxib mitigates genotoxicity induced by ionizing radiation in human blood lymphocytes.Research in pharmaceutical sciences · 2017Article
- Dephosphorylation of Tak1 at Ser412 greatly contributes to the spermatocyte-specific testis toxicity induced by (5R)-5-hydroxytriptolide in C57BL/6 mice.Toxicology research · 2016Article
- Thromboxane A2 exerts promoting effects on cell proliferation through mediating cyclooxygenase-2 signal in lung adenocarcinoma cells.Journal of cancer research and clinical oncology · 2014Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Abstract Different cyclooxygenase (COX)-2 inhibitors were known to cause different cell cycle changes. We investigated whether this different effect on cell cycle change was due to concentration-dependent effect. We investigated the effects of celecoxib, a COX-2 selective inhibitor, on cell cycle regulation in irradiated cancer cells that express high or low levels of COX-2. Four stably COX-2 knocked-down or overexpressed cell lines were treated with various concentrations of celecoxib with or without radiation. Celecoxib differentially modulated the cell cycle according to the concentrations applied. G1 arrest was induced at lower concentrations, whereas G2/M arrest was induced at higher concentrations in each cell line tested. Radiation-induced G2/M arrest was enhanced at lower concentrations but reduced at higher concentrations. The cutoff values to divide lower and higher concentrations were cell-type specific. Celecoxib treatment activated Cdc25C and inhibited p21 expression in both unirradiated and irradiated cells, regardless of COX-2 expression. Apoptosis was induced in irradiated cells 48 hours after treatment with celecoxib dependent of COX-2. These results imply that celecoxib deactivates the G2 checkpoint via both Cdc25C- and p21-dependent pathways in irradiated cells, which subsequently die by secondary apoptosis. Cell cycle modulating effects in irradiated cells resulting from treatment with celecoxib may have clinical importance with regard to the potential application of celecoxib in cancer patients undergoing radiotherapy.
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