ArticleJournal of cancer research and clinical oncology2006
5-(4-chlorophenyl)-1-(4-methoxyphenyl)-3-trifluoromethylpyrazole acts in a reactive oxygen species-dependent manner to suppress human lung cancer growth.
Article in Journal of cancer research and clinical oncology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 39 citations in OpenAlex.
- Article
- One-Pot (3 + 2) Cycloaddition-Isomerization-Oxidation of 2,2,2-Trifluorodiazoethane and Styryl Derivatives.The Journal of organic chemistry · 2023Article
- One-Pot Synthesis of 1-Aryl-3-trifluoromethylpyrazoles Using Nitrile Imines and Mercaptoacetaldehyde As a Surrogate of Acetylene.Organic letters · 2023Article
- Cyclooxygenase-1 (COX-1) and COX-1 Inhibitors in Cancer: A Review of Oncology and Medicinal Chemistry Literature.Pharmaceuticals (Basel, Switzerland) · 2018Review
- Alpha-tocopheryl succinate potentiates the paclitaxel-induced apoptosis through enforced caspase 8 activation in human H460 lung cancer cells.Experimental & molecular medicine · 2009Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purpose5-(4-chlorophenyl)-1-(4-methoxyphenyl)-3-trifluoromethylpyrazole (SC-560) is a structural analog of celecoxib. Recent studies suggested that SC-560 inhibits the in vivo proliferation of colon and breast cancer cells to an extent similar to that observed in celecoxib, and that SC-560 exerts their growth inhibitory effects in a cyclooxygenase-independent manner.
methodsIn the current study, we sought to investigate the mechanism by which SC-560 inhibits the growth of human lung cancer cells.
resultsSC-560 more potently inhibited the growth of human A549, H460, and H358 lung cancer cell lines compared with that of human BEAS-2B normal bronchial epithelial cells. SC-560-induced growth inhibition was mainly due to the induction of cell-cycle arrest at the G1 phase without apoptosis induction. SC-560 rapidly and dose-dependently induced the generation of reactive oxygen species (ROS), followed by accumulation of cells at the G1 phase. Antioxidant pretreatment blocked the cell-cycle arrest and growth inhibition induced by SC-560. Combination treatment with other ROS-inducing agents such as alpha-tocopheryl succinate (TOS) augmented cellular response against SC-560, leading to synergistic apoptosis induction and growth suppression. Our data also showed that the apoptosis induced by combination treatment with SC-560 and TOS was mediated through ROS-dependent caspase activation.
conclusionCollectively, our results demonstrate that SC-560 acts in a ROS-dependent manner to induce growth suppression in human lung cancer cells.
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