Please use this identifier to cite or link to this item: http://hdl.handle.net/10553/43485
Title: Inhibition of proliferation and induction of apoptosis by melatonin in human myeloid HL-60 cells
Authors: Rubio Sánchez, Sara 
Estevez, Francisco 
Cabrera, Javier
Reiter, Russel J.
Loro, Juan 
Quintana, Jose 
UNESCO Clasification: 32 Ciencias médicas
Keywords: Apoptosis
Cell cycle
Cellproliferation
HL-60 cells
Melatonin
Issue Date: 2007
Publisher: 0742-3098
Project: Subvenciones Para Equipamiento E Infraestructura Científico-Tecnológica de Las Universidades Canarias y de Sus Centros E Institutos Universitarios de Investigación, Con Financiación Feder, Para El Ejercicio 2005 
Síntesis y Evaluación Antitumoral de Nuevos Compuestos Con Un Grupo A-Metilen-G-Butirolactona. 
Journal: Journal of Pineal Research 
Abstract: Melatonin is an indoleamine that is synthesized in the pineal glandand has an extensive repertoire of biological activities. In the present study,we found that melatonin reduced the growth of the human myeloid leukemiacells HL-60, inhibiting progression from G1toSphaseofthecellcycleandincreasing apoptotic cell death. Furthermore, melatonin treatment elevatedcytochromecrelease from mitochondria and augmented caspase-3 andcaspase-9 activities. Upregulation of Bax and downregulation of Bcl-2 wasalso observed upon melatonin treatment. The effects of melatonin werefound not to be mediated by membrane receptors for the indoleamine.Together, our results suggest that melatonin reduces the viability of HL-60cells via induction of apoptosis primarily through regulation of Bax/Bcl-2expression.
URI: http://hdl.handle.net/10553/43485
ISSN: 0742-3098
DOI: 10.1111/j.1600-079X.2006.00392.x
Source: Journal Of Pineal Research [ISSN 0742-3098], v. 42 (2), p. 131-138
Appears in Collections:Artículos
Show full item record

SCOPUSTM   
Citations

82
checked on Apr 14, 2024

WEB OF SCIENCETM
Citations

77
checked on Feb 25, 2024

Page view(s)

78
checked on Mar 23, 2024

Google ScholarTM

Check

Altmetric


Share



Export metadata



Items in accedaCRIS are protected by copyright, with all rights reserved, unless otherwise indicated.