ArticleOncogene2007
Stat5 activation inhibits prolactin-induced AP-1 activity: distinct prolactin-initiated signals in tumorigenesis dependent on cell context.
Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
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
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.
- Expression and prognostic role of STAT5a across cancer types.Bioscience reports · 2023Pooled it
- The potential role of targeting the leptin receptor as a treatment for breast cancer in the context of hyperleptinemia: a literature review.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Association of Selected STAT Inhibitors with Prolactin-Induced Protein (PIP) in Breast Cancer.International journal of molecular sciences · 2025Article
- Cryoablation of primary breast cancer tumors induces a systemic abscopal effect altering TIME (Tumor Immune Microenvironment) in distant tumors.Frontiers in immunology · 2024Article
- Prolactin: The Third Hormone in Breast Cancer.Frontiers in endocrinology · 2022Review
- Involvement of STAT5 in Oncogenesis.Biomedicines · 2020Review
- 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
- Elevated collagen-I augments tumor progressive signals, intravasation and metastasis of prolactin-induced estrogen receptor alpha positive mammary tumor cells.Breast cancer research : BCR · 2017Article
- Prolactin signaling through focal adhesion complexes is amplified by stiff extracellular matrices in breast cancer cells.Oncotarget · 2016Article
- Prolactin Signaling Stimulates Invasion via Na(+)/H(+) Exchanger NHE1 in T47D Human Breast Cancer Cells.Molecular endocrinology (Baltimore, Md.) · 2016Article
- IL-8 induces miR-424-5p expression and modulates SOCS2/STAT5 signaling pathway in oral squamous cell carcinoma.Molecular oncology · 2016Article
- Signal transducer and activator of transcription 3 and 5 regulate system Xc- and redox balance in human breast cancer cells.Molecular and cellular biochemistry · 2015Article
- Tyrosyl phosphorylated serine-threonine kinase PAK1 is a novel regulator of prolactin-dependent breast cancer cell motility and invasion.Advances in experimental medicine and biology · 2015Review
- 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
- Article
- An N-terminal splice variant of human Stat5a that interacts with different transcription factors is the dominant form expressed in invasive ductal carcinoma.Cancer letters · 2014Article
- Reevaluation of the proposed autocrine proliferative function of prolactin in breast cancer.Breast cancer research and treatment · 2013Article
- The inhibition of stat5 by a Peptide aptamer ligand specific for the DNA binding domain prevents target gene transactivation and the growth of breast and prostate tumor cells.Pharmaceuticals (Basel, Switzerland) · 2013Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The essential role of prolactin (PRL) in normal mammary gland growth and differentiation has implicated this hormone in the development and progression of breast cancer. Although Stat5 is the best-characterized mediator of PRL signals, PRL also activates multiple other signals, whose roles in normal and pathologic processes are not well understood. We have shown that PRL stimulates activating protein-1 (AP-1) activity in breast cancer cells, and can cooperate with estradiol in this pathway. AP-1 modulates many processes critical for carcinogenesis, including cell proliferation, survival, transformation, invasion and angiogenesis, and is elevated in many neoplasms, including breast tumors. Here, we investigated the relationship between PRL signals to AP-1 and Stat5. We found that PRL activation of Stat5a and Stat5b, but not Stat1 or Stat3, reduced PRL signals to AP-1, without altering estradiol-induced AP-1 activity. The truncation mutant, Stat5/Delta53C, but not Stat5Y699F, was an effective inhibitor, consistent with a requirement for Stat5 dimerization and nuclear accumulation, but not its C-terminal transactivation activity. The association of Stat5 with AP-1 proteins suggests that this underlies the inhibition. Predictably, the ability of PRL to activate Stat5 and AP-1 was inversely related in mammary cell lines. Further, reduction of Stat5 protein with siRNA in T47D cells, which contain elevated Stat5, increased PRL-induced AP-1 signals, transcripts for the AP-1 target, matrix metalloproteinase-2 and associated invasive behavior. This study points to the importance of cell context in determining the spectrum of PRL-induced actions, which is critical for understanding the contributions of PRL to breast cancer.
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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.