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Inhibition of proliferation and induction of apoptosis by melatonin in human myeloid HL‐60 cells
Author(s) -
Rubio Sara,
Estévez Francisco,
Cabrera Javier,
Reiter Russel J.,
Loro Juan,
Quintana José
Publication year - 2007
Publication title -
journal of pineal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.881
H-Index - 131
eISSN - 1600-079X
pISSN - 0742-3098
DOI - 10.1111/j.1600-079x.2006.00392.x
Subject(s) - melatonin , downregulation and upregulation , apoptosis , mitochondrion , biology , pineal gland , myeloid , myeloid leukemia , cell growth , microbiology and biotechnology , melatonin receptor , medicine , viability assay , endocrinology , cancer research , biochemistry , gene
Melatonin is an indoleamine that is synthesized in the pineal gland and has an extensive repertoire of biological activities. In the present study, we found that melatonin reduced the growth of the human myeloid leukemia cells HL‐60, inhibiting progression from G 1 to S phase of the cell cycle and increasing apoptotic cell death. Furthermore, melatonin treatment elevated cytochrome c release from mitochondria and augmented caspase‐3 and caspase‐9 activities. Upregulation of Bax and downregulation of Bcl‐2 was also observed upon melatonin treatment. The effects of melatonin were found not to be mediated by membrane receptors for the indoleamine. Together, our results suggest that melatonin reduces the viability of HL‐60 cells via induction of apoptosis primarily through regulation of Bax/Bcl‐2 expression.