<td class= (Institución)
   (Nuevo usuario)
Ayuda  | Contacto  |  Castellano English  

Dadun > Depósito Académico > CIMA (Centro de Investigación Médica Aplicada) > Área de Oncología > Biomarcadores > DA - CIMA - Oncología - Biomarcadores - Artículos de Revista >

Adrenomedullin inhibits prostate cancer cell proliferation through a cAMP-independent autocrine mechanism
Autor(es) : Abasolo, I. (Ibane)
Wang, Z. (Zhou)
Montuenga, L.M. (Luis M.)
Calvo, A. (Alfonso)
Palabras clave : Adrenomedullin
Prostate cancer
Growth inhibition
Fecha incorporación: 2004
Editorial : Elsevier
Versión del editor: http://www.sciencedirect.com/science/article/pii/S0006291X04017371
ISSN: 1090-2104
Cita: Abasolo I, Wang Z, Montuenga LM, Calvo A. Adrenomedullin inhibits prostate cancer cell proliferation through a cAMP-independent autocrine mechanism. Biochem Biophys Res Commun 2004 Sep 24;322(3):878-886.
Adrenomedullin (AM) is a multifunctional peptide expressed in the normal and malignant prostate, and in prostate cancer cells. To elucidate the potential role of AM in prostate cancer, we have transfected the human AM gene into PC-3, DU 145, and LNCaP prostate cancer cells. Northern blot, Western blot, and radioimmunoassay techniques confirmed an increase in the synthesis and secretion of the 6kDa mature peptide, in the AM-transfected clones. Proliferation and cell cycle assays demonstrated that AM overexpression inhibited cell proliferation in PC-3 and LNCaP cells through a G0/G1 cell cycle arrest, but not in DU 145 cells. In vivo growth assays also confirmed that, at least in PC-3, AM produced a very significant reduction of tumor volume. In addition, the three cell lines expressed the CL/RCP/RAMP-2 receptor complex by RT-PCR, which suggests that AM peptide acts through an autocrine loop in prostate cancer cells. Although cAMP elevation is the most common pathway involved in AM signalling, stimulation of PC-3, DU 145, and LNCaP with synthetic AM did not increase intracellular cAMP. However, short-term stimulation of PC-3 cells with synthetic AM increased ERK1/2 activation. On the contrary, long-term stimulation, or AM overexpression, caused a reduction in the basal activation of ERK1/2. In summary, our results demonstrate that AM (either overexpressed or exogenously added) causes an inhibition of prostate cancer cell growth. This inhibition does not depend on changes in intracellular cAMP levels, but may be related to ERK1/2 activation.
Enlace permanente: http://hdl.handle.net/10171/18808
Aparece en las colecciones: DA - CIMA - Oncología - Nuevas dianas terapéuticas - Artículos de revista
DA - Ciencias - HAP - Artículos de revista
DA - CIMA - Oncología - Biomarcadores - Artículos de Revista

Ficheros en este registro:
Fichero:  15Abasolo BBRC 2004.pdf
Tamaño:  3,41 MB
Formato:  Adobe PDF
 Visualizar / Abrir 

Los ítems de Dadun están protegidos por copyright, con todos los derechos reservados, a menos que se indique lo contrario.