ArticleEndocrinology2013
Prolactin activates ERα in the absence of ligand in female mammary development and carcinogenesis in vivo.
Article in Endocrinology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 24 citations in OpenAlex.
- The influence of two neurohormones on breast cancer: prolactin and melatonin.Revista da Associacao Medica Brasileira (1992) · 2025Article
- Breast Cancer and Prolactin - New Mechanisms and Models.Endocrinology · 2022Review
- Prolactin receptor signaling: A novel target for cancer treatment - Exploring anti-PRLR signaling strategies.Frontiers in endocrinology · 2022Review
- Prolactin: The Third Hormone in Breast Cancer.Frontiers in endocrinology · 2022Review
- Prolactin and endocrine therapy resistance in breast cancer: The next potential hope for breast cancer treatment.Journal of cellular and molecular medicine · 2021Review
- Prolactin synergizes with canonical Wnt signals to drive development of ER+ mammary tumors via activation of the Notch pathway.Cancer letters · 2021Article
- Interaction between 17β-estradiol, prolactin and human papillomavirus induce E6/E7 transcript and modulate the expression and localization of hormonal receptors.Cancer cell international · 2019Article
- Unraveling the action mechanism ofAmerican journal of translational research · 2019Article
- Chi-miR-3031 regulates beta-casein via the PI3K/AKT-mTOR signaling pathway in goat mammary epithelial cells (GMECs).BMC veterinary research · 2018Article
- 17Journal of the Endocrine Society · 2018Article
- Prolactin Alters the Mammary Epithelial Hierarchy, Increasing Progenitors and Facilitating Ovarian Steroid Action.Stem cell reports · 2017Article
- Article
- Mammary gland development--It's not just about estrogen.Journal of dairy science · 2016Review
- Hormone-sensing mammary epithelial progenitors: emerging identity and hormonal regulation.Journal of mammary gland biology and neoplasia · 2015Review
- Minireview: Tipping the balance: ligand-independent activation of steroid receptors.Molecular endocrinology (Baltimore, Md.) · 2015Review
- Modeling prolactin actions in breast cancer in vivo: insights from the NRL-PRL mouse.Advances in experimental medicine and biology · 2015Article
- Article
- Genetically engineered ERα-positive breast cancer mouse models.Endocrine-related cancer · 2014Review
- Effects of parity and serum prolactin levels on the incidence and regression of DMBA-induced tumors in OFA hr/hr rats.BioMed research international · 2014Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Resistance of estrogen receptor positive (ERα+) breast cancers to antiestrogens is a major factor in the mortality of this disease. Although activation of ERα in the absence of ligand is hypothesized to contribute to this resistance, the potency of this mechanism in vivo is not clear. Epidemiologic studies have strongly linked prolactin (PRL) to both development of ERα+ breast cancer and resistance to endocrine therapies. Here we employed genetically modified mouse models to examine the ability of PRL and cross talk with TGFα to activate ERα, using a mutated ERα, ERα(G525L), which is refractory to endogenous estrogens. We demonstrate that PRL promotes pubertal ERα-dependent mammary ductal elongation and gene expression in the absence of estrogen, which are abrogated by the antiestrogen, ICI 182,780 (ICI). PRL and TGFα together reduce sensitivity to estrogen, and 30% of their combined stimulation of ductal proliferation is inhibited by ICI, implicating ligand-independent activation of ERα as a component of their interaction. However, PRL/TGFα-induced heterogeneous ERα+ tumors developed more rapidly in the presence of ICI and contained altered transcripts for surface markers associated with epithelial subpopulations and increased signal transducer and activator of transcription 5b expression. Together, these data support strong interactions between PRL and estrogen on multiple levels. Ligand-independent activation of ERα suggests that PRL may contribute to resistance to antiestrogen therapies. However, these studies also underscore ERα-mediated moderation of tumor phenotype. In light of the high expression of PRL receptors in ERα+ cancers, understanding the actions of PRL and cross talk with other oncogenic factors and ERα itself has important implications for therapeutic strategies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.