ArticleMolecular endocrinology (Baltimore, Md.)2004
Multiple kinase cascades mediate prolactin signals to activating protein-1 in breast cancer cells.
Article in Molecular endocrinology (Baltimore, Md.), 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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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.
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.
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Who cites it
22 citing papers in PubMed, 42 citations in OpenAlex.
- Delaying Effects of Prolactin and Growth Hormone on Aging Processes in Bovine Oocytes Matured In Vitro.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Identification of an AP1-ZFP36 Regulatory Network Associated with Breast Cancer Prognosis.Journal of mammary gland biology and neoplasia · 2020Article
- 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
- Modeling prolactin actions in breast cancer in vivo: insights from the NRL-PRL mouse.Advances in experimental medicine and biology · 2015Article
- Prolactin and growth hormone affect metaphase-II chromosomes in aging oocytes via cumulus cells using similar signaling pathways.Frontiers in genetics · 2015Article
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- Mechanisms of transient signaling via short and long prolactin receptor isoforms in female and male sensory neurons.The Journal of biological chemistry · 2013Article
- PAK1 regulates breast cancer cell invasion through secretion of matrix metalloproteinases in response to prolactin and three-dimensional collagen IV.Molecular endocrinology (Baltimore, Md.) · 2013Article
- Stiff collagen matrices increase tumorigenic prolactin signaling in breast cancer cells.The Journal of biological chemistry · 2013Article
- PAK1-Nck regulates cyclin D1 promoter activity in response to prolactin.Molecular endocrinology (Baltimore, Md.) · 2011Article
- Prolactin-induced mouse mammary carcinomas model estrogen resistant luminal breast cancer.Breast cancer research : BCR · 2011Article
- Ovarian hormones are not required for PRL-induced mammary tumorigenesis, but estrogen enhances neoplastic processes.The Journal of endocrinology · 2009Article
- Complex prolactin crosstalk in breast cancer: new therapeutic implications.Molecular and cellular endocrinology · 2009Article
- Tyrosine phosphorylation of Grb2: role in prolactin/epidermal growth factor cross talk in mammary epithelial cell growth and differentiation.Molecular and cellular biology · 2009Article
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- Prolactin-growth factor crosstalk reduces mammary estrogen responsiveness despite elevated ERalpha expression.The American journal of pathology · 2009Article
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- Prolactin receptor antagonism reduces the clonogenic capacity of breast cancer cells and potentiates doxorubicin and paclitaxel cytotoxicity.Breast cancer research : BCR · 2008Article
- Prolactin, TNF alpha and nitric oxide expression in nitroso-N-methylurea-induced-mammary tumours.Journal of carcinogenesis · 2007Article
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Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The importance of prolactin (PRL) in physiological proliferation and differentiation of the mammary gland, together with high levels of PRL receptors in breast tumors, the association of circulating PRL with incidence of breast cancer, and the recognition of locally produced PRL, point to the need for greater understanding of PRL actions in mammary disease. Although PRL has been shown to activate multiple kinase cascades in various target cells, relatively little is known of its signaling pathways in the mammary gland apart from the Janus kinase 2/ signal transducer and activator of transcription 5 pathway, particularly in tumor cells. Another potential effector is activating protein-1 (AP-1), a transcription complex that regulates processes essential for neoplastic progression, including proliferation, survival and invasion. We demonstrate that PRL activates AP-1 in MCF-7 cells, detectable at 4 h and sustained for at least 24 h. Although Janus kinase 2 and ERK1/2 are the primary mediators of PRL-induced signals, c-Src, phosphatidylinositol 3'-kinase, protein kinase C, and other MAPKs contribute to maximal activity. PRL activation of these pathways leads to increased c-Jun protein and phosphorylation, JunB protein, and phosphorylation of c-Fos, elevating the levels of AP-1 complexes able to bind DNA. These active AP-1 dimers may direct expression of multiple target genes, mediating some of PRL's actions in mammary disease.
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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.