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Título: Farnesoid X Receptor (FXR) from normal to malignant state
Fecha de publicación: 2012
Editorial: F. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología
Cita bibliográfica: Histology and histopathology, Vol. 27, nº 7 (2012)
ISSN: 1699-5848
0213-3911
Materias relacionadas: CDU::6 - Ciencias aplicadas::61 - Medicina
CDU::6 - Ciencias aplicadas::61 - Medicina::615 - Farmacología. Terapéutica. Toxicología. Radiología
Palabras clave: Bile acid
Inflammation
Resumen: The Farnesoid X Receptor (FXR) is a member of the nuclear receptor superfamily of ligand-activated transcription factors, which plays crucial role in bile acid, cholesterol, lipid and glucose metabolism, as well as in the development of atherosclerosis, intestinal bacterial growth and liver regeneration. FXR is also involved in the pathogenesis of cholestatic diseases, non-alcoholic fatty liver disease and inflammatory bowel disease. Recent evidence further suggests a key role for FXR in apoptosis and cancer. Notably, FXR deficiency promoted intestinal inflammation and tumorigenesis, suggesting that FXR activation might be a promising strategy in the treatment of colon cancer. FXR deficiency in mice led to the development of spontaneous hepatocarcinomas, while FXR inhibition might represent a novel therapeutic approach in Barett’s esophagus. In breast cancer cell lines, FXR agonists down-regulated the breast cancer target gene aromatase. FXR inhibited Leydig tumor growth and progression, supporting evidence that FXR may be an important regulator of androgen homoeostasis. Further studies are required in order to establish possible antitumor effects of this nuclear receptor. Either reactivating or inhibiting FXR expression may represent promising therapeutic strategies in the treatment of certain types of human cancer
Autor/es principal/es: Koutsounas, Loannis
Giaginis, Constantinos
Theocharis, Stamatios
URI: http://hdl.handle.net/10201/54068
Tipo de documento: info:eu-repo/semantics/article
Número páginas / Extensión: 19
Derechos: info:eu-repo/semantics/openAccess
Aparece en las colecciones:Vol.27, nº 7 (2012)

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