Carcinogenesis, Vol 19, 1895-1900, Copyright © 1998 by Oxford University Press
WS Baldwin, GS Travlos, JI Risinger and JC Barrett
Melatonin, an indolic pineal hormone, is produced primarily at night in
mammals and is important in controlling biological rhythms. Previous
research suggested that melatonin can attenuate proliferation in the
estrogen-responsive MCF-7 breast cancer cell line. We tested whether these
anti-proliferative effects may have physiological consequences upon two
estrogen-responsive cell lines, MCF-7 (a breast cancer cell line) and BG-1
(an ovarian adenocarcinoma cell line). Melatonin (10(-9)- 10(-5) M)
attenuated proliferation of MCF-7 and BG-1 cells by >20% in the absence
of estrogen. However, 17beta-estradiol exposure negated the ability of
melatonin to inhibit proliferation. To substantiate this finding, cells
were estrogen starved followed by multiple treatments with estradiol and
melatonin. Melatonin did not inhibit estradiol- stimulated proliferation
under this protocol. Estradiol increased MCF-7 and BG-1 cell cycle
transition from G1 to S phase, however, melatonin did not inhibit this
transition nor did it down-regulate estradiol- induced pS2 mRNA levels
measured by northern blotting, further indicating that melatonin was unable
to attenuate estradiol-induced proliferation and gene expression. We also
examined the effects of melatonin on estradiol-induced proliferation in
MCF-7 cell xenografts in athymic nude mice. Melatonin at a dose 28 times
greater than 17beta- estradiol did not inhibit estradiol-induced
proliferation in vivo. Furthermore, pinealectomy did not increase
proliferation. Therefore, we conclude that melatonin does not directly
inhibit estradiol-induced proliferation.
ARTICLES
Melatonin does not inhibit estradiol-stimulated proliferation in MCF-7 and BG-1 cells
Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA.
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  S. J. London, J. M. Pogoda, K. L. Hwang, B. Langholz, K. R. Monroe, L. N. Kolonel, W. T. Kaune, J. M. Peters, and B. E. Henderson Residential Magnetic Field Exposure and Breast Cancer Risk: A Nested Case-Control Study from a Multiethnic Cohort in Los Angeles County, California Am. J. Epidemiol., November 15, 2003; 158(10): 969 - 980. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. K. Balcer-Kubiczek, G. H. Harrison, J.-F. Xu, and P. L. Gutierrez Coordinate Late Expression of Trefoil Peptide Genes (pS2/TFF1 and ITF/TFF3) in Human Breast, Colon, and Gastric Tumor Cells Exposed to X-Rays Mol. Cancer Ther., April 1, 2002; 1(6): 405 - 415. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. S. Schernhammer, F. Laden, F. E. Speizer, W. C. Willett, D. J. Hunter, I. Kawachi, and G. A. Colditz Rotating Night Shifts and Risk of Breast Cancer in Women Participating in the Nurses' Health Study J Natl Cancer Inst, October 17, 2001; 93(20): 1563 - 1568. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Ishido, H. Nitta, and M. Kabuto Magnetic fields (MF) of 50 Hz at 1.2 {micro}T as well as 100 {micro}T cause uncoupling of inhibitory pathways of adenylyl cyclase mediated by melatonin 1a receptor in MF-sensitive MCF-7 cells Carcinogenesis, July 1, 2001; 22(7): 1043 - 1048. [Abstract] [Full Text] [PDF]
|
|