EGF stimulates Pit-1 independent transcription of the human prolactin pituitary promoter in human breast cancer SK-BR-3 cells through its proximal AP-1 response element

Manfroid, Isabelle; Weerdt, Cécile Van de; Baudhuin, Ariane; Martial, Joseph; Müller, Marc

doi:10.1016/j.mce.2004.08.009

Cited by 18 publications

(11 citation statements)

References 53 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, some extrapituitary tissues and cell lines, such as prostate cancer cells and the human breast adenocarcinoma cells, SK-BR-3, do not express Pit-1, yet PRL transcripts corresponding to the proximal promoter are present (Shaw-Bruha et al . 1997, Manfroid et al . 2005, Dagvadorj et al .…”

Section: Discussionmentioning

confidence: 99%

The Pit-1/Pou1f1 transcription factor regulates and correlates with prolactin expression in human breast cell lines and tumors

Ben-Batalla¹,

Seoane²,

Macı́a³

et al. 2010

Endocrine-Related Cancer

View full text Add to dashboard Cite

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.

show abstract

Section: Discussionmentioning

confidence: 99%

The Pit-1/Pou1f1 transcription factor regulates and correlates with prolactin expression in human breast cell lines and tumors

Ben-Batalla¹,

Seoane²,

Macı́a³

et al. 2010

Endocrine-Related Cancer

View full text Add to dashboard Cite

show abstract

“…Indeed, while PRL mRNA transcribed from the extrapituitary promoter is w150 bp longer compared with that transcribed from the pituitary promoter, both mRNA were shown to occur in various human breast/prostate cancer cell lines or biopsies (ShawBruha et al 1997, Dagvadorj et al 2007. Moreover, it has been shown that in the SK-BR-3 human mammary tumor cell line, the sole pituitary promoter was active, despite of the absence of Pit-1 in mammary cells (Manfroid et al 2005). Whatever our still limited understanding of PRL promoter usage, the rareness of extrapituitary PRL gene expression in rodents led to the fact that local PRL escaped (almost) all non-genetically modified animal models (see below).…”

Section: Prl Not Only An Endocrine Hormonementioning

confidence: 99%

New concepts in prolactin biology

Bernichtein

Touraine²,

Goffin³

2010

Journal of Endocrinology

154

112

View full text Add to dashboard Cite

Human prolactin (PRL) is currently viewed as a hormone of pituitary origin, whose production (i.e. serum levels) is controlled by dopamine, whose biological actions relate exclusively to lactation and reproductive functions, for which any genetic disorder is yet to be identified, and whose unique associated pathology is hyperprolactinemia. Both experimental studies and human sample/cohort-based investigations performed during the past decade have considerably widened our perception of PRL biology: i) there are now strong epidemiological arguments supporting the fact that circulating PRL is a risk factor for breast cancer, ii) in addition to the endocrine hormone, locally produced PRL has been documented in several human tissues; there is increasing evidence supporting the tumor growth potency of local PRL, acting via autocrine/paracrine mechanisms, in both rodent models, and human breast and prostate tumors, iii) the first functional germinal polymorphisms of the PRL receptor were recently identified in patients presenting with breast tumors, which involve single amino acid substitution variants exhibiting constitutive activity, iv) human PRL analogs have been engineered, which were shown in experimental models to down-regulate the effects triggered by local PRL (competitive antagonism) or by the constitutively active receptor variants (inverse agonism). The aim of this review is to discuss these novel concepts in PRL biology, including their potential pathophysiological outcomes.

show abstract

“…promoter usage (91). Still more surprising, a recent study has shown that in the SK-BR-3 human mammary tumor cell line, the pituitary promoter, and not the decidual/lymphocyte promoter, is active, despite the absence of Pit-1 in mammary cells (92). In view of these two studies, the alternative promoter usage in pituitary vs. nonpituitary tissues is a concept that obviously needs to be revisited.…”

Section: Regulation Of Autocrine Prl Expressionmentioning

confidence: 99%

Development and Potential Clinical Uses of Human Prolactin Receptor Antagonists

et al. 2005

View full text Add to dashboard Cite

There is a large body of literature showing that prolactin (PRL) exerts growth-promoting activities in breast cancer, and possibly in prostate cancer and prostate hyperplasia. In addition, increasing evidence argues for the involvement of locally produced (autocrine) PRL, perhaps even more than pituitary-secreted (endocrine) PRL, in tumor growth. Because dopamine analogs are unable to inhibit PRL production in extrapituitary sites, alternative strategies need investigation. To that end, several PRL receptor antagonists have been developed by introducing various mutations into its natural ligands. For all but one of these analogs, the mechanism of action involves a competition with endogenous PRL for receptor binding. Such compounds are thus candidates to counteract the undesired actions of PRL, not only in tumors, but also in dopamine-resistant prolactinomas. In this review, we describe the different versions of antagonists that have been developed, with emphasis on the controversies regarding their characterization, and the limits for their potential development as a drug. The most recently developed antagonist, Delta1-9-G129R-hPRL, is the only one that is totally devoid of residual agonistic activity, meaning it acts as pure antagonist. We discuss to what extent this new molecule could be considered as a lead compound for inhibiting the actions of human PRL in the above-mentioned diseases. We also speculate on the multiple questions that could be addressed with respect to the therapeutic use of PRL receptor antagonists in patients.

show abstract

EGF stimulates Pit-1 independent transcription of the human prolactin pituitary promoter in human breast cancer SK-BR-3 cells through its proximal AP-1 response element

Cited by 18 publications

References 53 publications

The Pit-1/Pou1f1 transcription factor regulates and correlates with prolactin expression in human breast cell lines and tumors

The Pit-1/Pou1f1 transcription factor regulates and correlates with prolactin expression in human breast cell lines and tumors

New concepts in prolactin biology

Development and Potential Clinical Uses of Human Prolactin Receptor Antagonists

Contact Info

Product

Resources

About