ArticleMolecular endocrinology (Baltimore, Md.)2011
CEBPD suppresses prolactin expression and prolactinoma cell proliferation.
Article in Molecular endocrinology (Baltimore, Md.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- Genomic analyses identify agents regulating somatotroph and lactotroph functions.Functional & integrative genomics · 2016Pooled it
- Basic biology and roles of CEBPD in cardiovascular disease.Cell death discovery · 2025Review
- Transcriptomic Profiles of Normal Pituitary Cells and Pituitary Neuroendocrine Tumor Cells.Cancers · 2022Review
- TRH Regulates the Synthesis and Secretion of Prolactin in Rats with Adenohypophysis through the Differential Expression of miR-126a-5p.International journal of molecular sciences · 2022Article
- Postnatal developmental trajectory of sex-biased gene expression in the mouse pituitary gland.Biology of sex differences · 2022Article
- Article
- CCAAT/enhancer binding protein δ is a transcriptional repressor of α-synuclein.Cell death and differentiation · 2020Article
- Natural and molecular history of prolactinoma: insights from aOncotarget · 2018Article
- Gene signatures of drug resistance predict patient survival in colorectal cancer.The pharmacogenomics journal · 2015Article
- The many faces of C/EBPδ and their relevance for inflammation and cancer.International journal of biological sciences · 2013Review
- Genomic characterization of human and rat prolactinomas.Endocrinology · 2012Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Hyperprolactinemia, usually caused by a pituitary lactotroph tumor, leads to galactorrhea and infertility. Increased prolactin (PRL) levels may be due to enhanced PRL expression or proliferation of PRL-secreting cells. We hypothesize that PRL expression and PRL-secreting cell proliferation are linked. Using microarray-based gene expression profiling, we identified CCAAT-enhancer-binding protein δ (CEBPD) transcription factor as a critical gene that regulates both PRL expression and lactotroph cell proliferation. CEBPD expression levels are decreased approximately 7-fold in experimental rat prolactinoma cells. Forced expression of this transcription factor in PRL-secreting cells (GH3 and MMQ) inhibited PRL expression and cellular proliferation, and CEBPD knockdown by small interfering RNA leads to increased PRL expression in both cell lines. To determine mechanisms underlying this observation, we determined binding of CEBPD to the PRL promoter and also showed marked suppression (96%) of PRL promoter activity. CEBPD and Pit1 interact and attenuate each other's binding to the PRL promoter. CEBPD also suppresses expression of proliferation-related genes, including c-Myc, survivin, as well as cyclins B1, B2, and D1. These results show that PRL expression and cell proliferation are controlled in part by CEBPD.
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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 Socratic graph.