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This version published online on March 3, 2005
Molecular Endocrinology, doi:10.1210/me.2004-0339
A more recent version of this article appeared on July 1, 2005
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*Breast Cancer

Submitted on August 30, 2004
Accepted on February 22, 2005

Prolactin and estrogen enhance the activity of Activating Protein-1 in breast cancer cells: role of ERK1/2-mediated signals to c-fos

Jennifer H. Gutzman, Sarah E. Nikolai, Debra E. Rugowski, Jyoti J. Watters, and Linda A. Schuler*

Molecular and Environmental Toxicology Program (J.H.G., L.A.S.) and Department of Comparative Biosciences (J.H.G., S.E.N., D.E.R., J.J.W., L.A.S.), University of Wisconsin-Madison, Madison, WI 53706

* To whom correspondence should be addressed. E-mail: schulerl{at}svm.vetmed.wisc.edu.

Despite the important roles of both prolactin (PRL) and 17{beta}-estradiol (E2) in normal mammary development as well as in breast cancer, and coexpression of the estrogen receptor (ER) and prolactin receptor (PRLR) in many mammary tumors, the interactions between PRL and E2 in breast cancer have not been well studied. The AP-1 transcription factor, a known regulator of processes essential for normal growth and development as well as carcinogenesis, is a potential site for crosstalk between these hormones in breast cancer cells. Here we demonstrate that PRL and E2 cooperatively enhance the activity of AP-1 in MCF-7-derived cells. In addition to the acute PRL-induced ERK1/2 activation, PRL and E2 also individually elicited delayed, sustained rises in levels of phosphorylated p38 and especially ERK1/2. Together, these hormones increased the dynamic phosphorylation of ERK1/2 and c-Fos, and induced c-fos promoter activity. Synergistic activation of the transcription factor, Elk-1, reflected the PRL-E2 interaction at ERK1/2, and is a likely mechanism for activation of the c-fos promoter via the SRE. The enhanced AP-1 activity resulting from the interaction of these hormones may increase expression of many target genes that are critical for oncogenesis and may contribute to neoplastic progression.
Key words: prolactin • estrogen • breast cancer • AP-1 • MCF-7

NURSA Molecule Pages Link:

Nuclear Receptors:   ERα
Ligands:   17β-Estradiol



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