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Inhibitory effects of pharmacological doses of melatonin on aromatase activity and expression in rat glioma cells.

Authors: Gonzalez, A  Martinez-Campa, C  Mediavilla, MD  Alonso-Gonzalez, C  Sanchez-Barcelo, EJ  Cos, S 
Citation: Gonzalez A, etal., Br J Cancer. 2007 Sep 17;97(6):755-60. Epub 2007 Aug 14.
Pubmed: (View Article at PubMed) PMID:17700567
DOI: Full-text: DOI:10.1038/sj.bjc.6603935

Melatonin exerts oncostatic effects on different kinds of neoplasias, especially on oestrogen-dependent tumours. Recently, it has been described that melatonin, on the basis of its antioxidant properties, inhibits the growth of glioma cells. Glioma cells express oestrogen receptors and have the ability to synthesise oestrogens from androgens. In the present study, we demonstrate that pharmacological concentrations of melatonin decreases the growth of C6 glioma cells and reduces the local biosynthesis of oestrogens, through the inhibition of aromatase, the enzyme that catalyses the conversion of androgens into oestrogens. These results are supported by three types of evidence. Firstly, melatonin counteracts the growth stimulatory effects of testosterone on glioma cells, which is dependent on the local synthesis of oestrogens from testosterone. Secondly, we found that melatonin reduces the aromatase activity of C6 cells, measured by the tritiated water release assay. Finally, by (RT)-PCR, we found that melatonin downregulates aromatase mRNA steady-state levels in these glioma cells. We conclude that melatonin inhibits the local production of oestrogens decreasing aromatase activity and expression. By analogy to the implications of aromatase in other forms of oestrogen-sensitive tumours, it is conceivable that the modulation of the aromatase by pharmacological melatonin may play a role in the growth of glioblastomas.


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CRRD Object Information
CRRD ID: 4890365
Created: 2010-12-15
Species: All species
Last Modified: 2010-12-15
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.