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This Article IMMEDIATE FREE ACCESS ARTICLE OA Free Full Text Full Text (PDF) OA All Versions of this Article: ERC-09-0100v1 17/1/73    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Ben-Batalla, I Articles by Perez-Fernandez, R PubMed PubMed Citation Articles by Ben-Batalla, I Articles by Perez-Fernandez, R

Departments of
¹ Physiology,
² Obstetrics and Gynecology
³ Morphological Sciences, School of Medicine, University Clinical Hospital, University of Santiago de Compostela, 15782 Santiago de Compostela, Spain
⁴ Unidad de Investigación del Hospital de Jove, 33920 Gijón, Spain

(Correspondence should be addressed to R Perez-Fernandez, Departamento de Fisiología, Facultad de Medicina, Universidad de Santiago de Compostela, 15782 Santiago de Compostela, Spain; Email: roman.perez.fernandez{at}usc.es)

This is an Open Access article distributed under the terms of the Society for Endocrinology's Re-use Licence which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

The transcription factor Pit-1/Pou1f1 regulates GH and prolactin (PRL) secretion in the pituitary gland. Pit-1 expression and GH regulation by Pit-1 have also been demonstrated in mammary gland. However, no data are available on the role of Pit-1 on breast PRL. To evaluate this role, several human breast cancer cell lines were transfected with either the Pit-1 expression vector or a Pit-1 small interference RNA construct, followed by PRL mRNA and protein evaluation. In addition, transient transfection of MCF-7 cells by a reporter construct containing the proximal PRL promoter, and ChIP assays were performed. Our data indicate that Pit-1 regulates mammary PRL at transcriptional level by binding to the proximal PRL promoter. We also found that Pit-1 raises cyclin D1 expression before increasing PRL levels, suggesting a PRL-independent effect of Pit-1 on cell proliferation. By using immunohistochemistry, we found a significant correlation between Pit-1 and PRL expression in 94 human breast invasive ductal carcinomas. Considering the possible role of PRL in breast cancer disorders, the function of Pit-1 in breast should be the focus of further research.