ArticleOncogene2000
Human prolactin (hPRL) antagonists inhibit hPRL-activated signaling pathways involved in breast cancer cell proliferation.
Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed, 105 citations in OpenAlex.
- Plasma prolactin and postmenopausal breast cancer risk: a pooled analysis of four prospective cohort studies.Breast cancer research : BCR · 2024Article
- Prolactin receptor signaling: A novel target for cancer treatment - Exploring anti-PRLR signaling strategies.Frontiers in endocrinology · 2022Review
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- Identification of NEK3 Kinase Threonine 165 as a Novel Regulatory Phosphorylation Site That Modulates Focal Adhesion Remodeling Necessary for Breast Cancer Cell Migration.The Journal of biological chemistry · 2016Article
- Role of EGF/ERBB1 in the transcriptional regulation of the prolactin receptor independent of estrogen and prolactin in breast cancer cells.Oncotarget · 2016Article
- GHR/PRLR Heteromultimer Is Composed of GHR Homodimers and PRLR Homodimers.Molecular endocrinology (Baltimore, Md.) · 2016Article
- An SH2 domain model of STAT5 in complex with phospho-peptides define "STAT5 Binding Signatures".Journal of computer-aided molecular design · 2015Article
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- Reevaluation of the proposed autocrine proliferative function of prolactin in breast cancer.Breast cancer research and treatment · 2013Article
- Prolactin gene expression in primary central nervous system tumors.Journal of negative results in biomedicine · 2013Article
- Prolactin regulation of the prostate gland: a female player in a male game.Nature reviews. Urology · 2011Review
- Signal transducer and activator of transcription 5a/b: biomarker and therapeutic target in prostate and breast cancer.The international journal of biochemistry & cell biology · 2011Review
- PAK1-Nck regulates cyclin D1 promoter activity in response to prolactin.Molecular endocrinology (Baltimore, Md.) · 2011Article
- Targeting transcription factor Stat5a/b as a therapeutic strategy for prostate cancer.American journal of translational research · 2011Article
- The Pit-1/Pou1f1 transcription factor regulates and correlates with prolactin expression in human breast cell lines and tumors.Endocrine-related cancer · 2010Article
- Intermediate Ca2+-sensitive K+ channels are necessary for prolactin-induced proliferation in breast cancer cells.The Journal of membrane biology · 2010Article
- Transcription factor Stat5a/b as a therapeutic target protein for prostate cancer.The international journal of biochemistry & cell biology · 2010Review
- Signal transducer and activator of transcription 5A/B in prostate and breast cancers.Endocrine-related cancer · 2008Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The involvement of human prolactin (hPRL) in breast cancer has been recently reconsidered based on its autocrine/paracrine proliferative effect described in human mammary tumor epithelial cells. Therefore, there is growing interest in the development of potent hPRL antagonists that may inhibit this effect. We previously designed hPRL analogs displaying antagonistic properties in a human transcriptional bioassay. We now report that the most potent of those analogs, G129R-hPRL, antagonizes all hPRL-induced effects analysed in various breast cancer cell lines, including cell proliferation. The analog per se lacks intrinsic agonistic activity on PRL receptor-activated signaling cascades, cell proliferation and apoptosis, indicating that its mode of action only occurs through competitive inhibition of hPRL. We provide some molecular basis of this antagonistic effect by demonstrating that G129R-hPRL competitively inhibits hPRL-activation of the JAK-STAT and MAPK pathways, two signaling cascades involved in the mitogenic effect of hPRL in mammary epithelial cells. This competitive inhibition persists for at least 48 h, as evidenced by long term analysis of STAT5b activation or of progression through cell cycle. These results are the first demonstration at the molecular level that hPRL antagonists interfering with receptor dimerization disrupt signaling events in breast cancer cells, which prevents hPRL-induced cell proliferation.
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What OpenQuestion holds
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.