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Título: Nonsteroidal anti-inflammatory drugs and oxidative stress in cancer cells
Fecha de publicación: 2007
Editorial: Murcia : F. Hernández
ISSN: 0213-3911
Materias relacionadas: 616 - Patología. Medicina clínica. Oncología
Palabras clave: NSAIDs
DNA
Resumen: Nonsteroidal antiinflammatory drugs (NSAIDs) induce apoptosis in a variety of cancer cells, including those of colon, prostate, breast and leukemia. In addition, the classical NSAIDs sulindac and aspirin are promising chemopreventive agents against colon cancer. NSAIDs inhibit cyclooxygenases (COX) preventing the formation of prostaglandins, prostacyclin and thromboxane. NSAIDs also exert other biological effects, including generation of reactive oxygen species (ROS) and inhibition of NF-kB-mediated signals. Despite many suggested mechanisms for their anticancer effects, it remains uncertain how they induce cell cycle arrest and apoptosis in cancer cells. Furthermore, there is little information on the selectivity of NSAIDs-mediated anticancer effects, although this is one of the most important issues in cancer therapy. Increased understanding of the biological basis for the anticancer activity of NSAIDs and their selectivity is essential for future therapeutic advances. In this paper, we propose that increased ROS generation is one of the key mechanisms for NSAIDs-mediated anticancer effects on various cancer cells.
Autor/es principal/es: Adachi, M.
Sakamoto, H.
Kawamura, R.
Wang, W.
Imai, K.
Shinomura, Y.
Forma parte de: Histology and histopathology
URI: http://hdl.handle.net/10201/27566
Tipo de documento: info:eu-repo/semantics/article
Número páginas / Extensión: 6
Derechos: info:eu-repo/semantics/openAccess
Aparece en las colecciones:Vol.22, nº 4 (2007)

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