ArticleThe American journal of pathology2013
The prolactin receptor transactivation domain is associated with steroid hormone receptor expression and malignant progression of breast cancer.
Article in The American journal of pathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 34 citations in OpenAlex.
- PathCLAST: pathway-augmented contrastive learning with attention for interpretable spatial transcriptomics.Briefings in bioinformatics · 2026Article
- BRPF1 in cancer epigenetics: a key regulator of histone acetylation and a promising therapeutic target.Cell death discovery · 2025Review
- Prolactin: The Third Hormone in Breast Cancer.Frontiers in endocrinology · 2022Review
- Medicinal MushroomEvidence-based complementary and alternative medicine : eCAM · 2022Article
- The Expression of Prolactin Receptors in Benign Breast Tumors Is Not Associated with Serum Prolactin Level.Journal of clinical medicine · 2021Article
- Serine residues 726 and 780 have nonredundant roles regulating STAT5a activity in luminal breast cancer.Scientific reports · 2021Article
- The human intermediate prolactin receptor is a mammary proto-oncogene.NPJ breast cancer · 2021Article
- The Relevant Participation of Prolactin in the Genesis and Progression of Gynecological Cancers.Frontiers in endocrinology · 2021Review
- Inhibition of the Activity of Cyclophilin A Impedes Prolactin Receptor-Mediated Signaling, Mammary Tumorigenesis, and Metastases.iScience · 2020Article
- 17Journal of the Endocrine Society · 2018Article
- Progesterone receptors (PR) mediate STAT actions: PR and prolactin receptor signaling crosstalk in breast cancer models.The Journal of steroid biochemistry and molecular biology · 2018Review
- Prolactin Alters the Mammary Epithelial Hierarchy, Increasing Progenitors and Facilitating Ovarian Steroid Action.Stem cell reports · 2017Article
- Histone H1 and Chromosomal Protein HMGN2 Regulate Prolactin-induced STAT5 Transcription Factor Recruitment and Function in Breast Cancer Cells.The Journal of biological chemistry · 2017Article
- HDAC6 Deacetylates HMGN2 to Regulate Stat5a Activity and Breast Cancer Growth.Molecular cancer research : MCR · 2016Article
- Truncating Prolactin Receptor Mutations Promote Tumor Growth in Murine Estrogen Receptor-Alpha Mammary Carcinomas.Cell reports · 2016Article
- Modeling prolactin actions in breast cancer in vivo: insights from the NRL-PRL mouse.Advances in experimental medicine and biology · 2015Article
- Dense collagen-I matrices enhance pro-tumorigenic estrogen-prolactin crosstalk in MCF-7 and T47D breast cancer cells.PloS one · 2015Article
- Global profiling of prolactin-modulated transcripts in breast cancer in vivo.Molecular cancer · 2013Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The polypeptide hormone prolactin (PRL) stimulates breast epithelial cell growth, differentiation, and motility through its cognate receptor, PRLr. PRLr is expressed in most breast cancers; however, its exact role remains elusive. Our laboratory previously described a novel mode of PRLr signaling in which Stat5a-mediated transcription is regulated through ligand-induced phosphorylation of the PRLr transactivation domain (TAD). Herein, we used a PRLr transactivation-deficient mutant (PRLrYDmut) to identify novel TAD-specific target genes. Microarray analysis identified 120 PRL-induced genes up-regulated by wild type but not PRLrYDmut. Compared with control, PRLr expression significantly induced expression of approximately 4700 PRL-induced genes, whereas PRLrYDmut ablated induction of all but 19 of these genes. Ingenuity pathway analysis found that the PRLr TAD most profoundly affected networks involving cancer and proliferation. In support of this, PRLrYDmut expression reduced anchorage-dependent and anchorage-independent growth. In addition, pathway analysis identified a link between the PRLr TAD and the estrogen and progesterone receptors (ERα/PR). Although neither ERα nor PR was identified as a PRL target gene, a TAD mutation significantly impaired ERα/PR expression and estrogen responsiveness. TMA analysis revealed a marked increase in nuclear, but not cytoplasmic, PRLr TAD phosphorylation as a function of neoplastic progression. We propose that PRLr TAD phosphorylation contributes to breast cancer pathogenesis, in part through regulation of ERα and PR, and has potential utility as a biomarker in this disease.
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Registered trials
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