Celecoxib prevents tumor growth in an animal model by a COX-2 independent mechanism

Content Provider	Semantic Scholar
Author	Bastos-Pereira, Amanda Leite Lugarini, Daiana Oliveira-Christoff, Adriana Ávila, Thiago Vinícius Teixeira, Simone Maria Pires, Amanda R. A. Muscará, Marcelo Nicolas Cadena, Silvia M. S. C. Donatti, Lucélia Assis, Helena Cristina Silva De Acco, Alexandra
Copyright Year	2009
Abstract	PurposeNonsteroidal antiinflammatory drugs (NSAIDs) have been shown to reduce cell growth in several tumors. Among these possible antineoplastic drugs are cyclooxygenase-2 (COX-2)-selective drugs, such as celecoxib, in which antitumoral mechanisms were evaluated in rats bearing Walker-256 (W256) tumor.MethodsW256 carcinosarcoma cells were inoculated subcutaneously (107 cells/rat) in rats submitted to treatment with celecoxib (25 mg kg−1) or vehicle for 14 days. Tumor growth, body-weight gain, and survival data were evaluated. The mechanisms, such as COX-2 expression and activity, oxidative stress, by means of enzymes and lipoperoxidation levels, and apoptosis mediators were also investigated.ResultsA reduction in tumor growth and an increased weight gain were observed. Celecoxib provided a higher incidence of survival compared with the control group. Cellular effects are probably COX-2 independent, because neither enzyme expression nor its activity, measured by tumoral PGE2, showed significant difference between groups. It is probable that this antitumor action is dependent on an apoptotic way, which has been evaluated by the expression of the antiapoptotic protein Bcl-xL, in addition to the cellular changes observed by electronic microscopy. Celecoxib has also a possible involvement with redox homeostasis, because its administration caused significant changes in the activity of oxidative enzymes, such as catalase and superoxide dismutase.ConclusionThese results confirm the antitumor effects of celecoxib in W256 cancer model, contributing to elucidating its antitumoral mechanism and corroborating scientific literature about its effect on other types of cancer.
Starting Page	267
Ending Page	276
Page Count	10
File Format	PDF HTM / HTML
DOI	10.1007/s00280-009-1031-8
PubMed reference number	19506872
Journal	Medline
Volume Number	65
Alternate Webpage(s)	http://www.inct-ta.furg.br/english/producao/242010.pdf
Alternate Webpage(s)	https://doi.org/10.1007/s00280-009-1031-8
Journal	Cancer Chemotherapy and Pharmacology
Language	English
Access Restriction	Open
Content Type	Text
Resource Type	Article