Evidence map›Paper›PMID 18832099›Full record

ArticleEndocrinology2009

Estrogen receptor-alpha mediates the epidermal growth factor-stimulated prolactin expression and release in lactotrophs.

Nira Ben-Jonathan, Shenglin Chen, Joseph A Dunckley, Christopher LaPensee, Sanjay Kansra

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.2field-weighted citation impact, top 8% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 41 citations in OpenAlex.

  1. EGFR/ErbB2-Targeting Lapatinib Therapy for Aggressive Prolactinomas.The Journal of clinical endocrinology and metabolism · 2021
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Nira Ben-JonathanDepartment of Cancer and Cell Biology, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.
Shenglin Chen
Joseph A Dunckley
Christopher LaPensee
Sanjay Kansra
University of Cincinnati Medical Center · USMedical College of Wisconsin · US

Funding

REPRODUCTIVE AND DEVELOPMENTAL TOXICOLOGY RESEARCHP30ES006096 · NIEHS · UNIVERSITY OF CINCINNATI · PI PINNEY, SUSAN MENGEL · 1992 to 2022
$35.4M
Training Program in Cancer TherapeuticsT32CA117846 · NCI · UNIVERSITY OF CINCINNATI · PI PRICE, CAROLYN M, TAKIAR, VINITA · 2006 to 2022
$6.5M
Prolactin as a Growth Factor in Breast CancerR01CA096613 · NCI · UNIVERSITY OF CINCINNATI · PI BEN-JONATHAN, NIRA · 2004 to 2013
$2.7M
Xenoestrogens: Genomic and Non-genomic MechanismsR01ES012212 · NIEHS · UNIVERSITY OF CINCINNATI · PI BEN-JONATHAN, NIRA · 2003 to 2006
$1.1M
NCI NIH HHS CA096613NCI NIH HHS R01 CA096613NCI NIH HHS T32 CA117846NIEHS NIH HHS ES012212NIEHS NIH HHS P30 ES006096NIEHS NIH HHS P30-ES06096NIEHS NIH HHS R01 ES012212
6 · The paper itself

Abstract

Epidermal growth factor (EGF) is a potent regulator of cell function in many cell types. EGF-receptor (EGFR/ErbB1)-activated Erk1/2 has been reported to activate estrogen receptor (ER) in an estrogen (E2)-independent manner. In the pituitary lactotrophs, both EGF and E2 stimulate prolactin (PRL) release, but the nature of interactions between ErbB and ERalpha signaling is unknown. Our objectives were to 1) characterize EGF-induced PRL release, 2) determine whether this effect requires ERalpha, and 3) determine the molecular basis for cross talk between ErbB and ERalpha signaling pathways. Using GH3 cells, a rat lactotroph cell line, we report that EGF stimulates PRL gene expression and release in a dose- and time-dependent manner. EGF caused a rapid and robust activation of Erk1/2 via ErbB1 and induced phosphorylation of S118 on ERalpha in an Erk1/2-dependent manner. The global antiestrogen ICI 182780 and the ERalpha-specific antagonist 1,3-bis(4-hydroxyphenyl)-4-methyl-5-[4-(2-piperidinylet hoxy)phenol]-1H-pyrazole dihydrochloride (MPP), but not the ERbeta-specific antagonist 4-[2-Phenyl-5,7-bis(trifluoromethyl) pyrazolo[1,5-a]pyrimidin-3-yl]phenol (PHTPP), blocked the EGF-induced PRL release, indicating an ERalpha requirement. This was further supported by using ERalpha knockdown by small interfering RNA. Because the antiestrogens did not block EGF-induced Mek-1 or Erk1/2 phosphorylation, ERalpha is placed downstream from the ErbB1-activated Erk1/2. These results provide the first evidence that ErbB1-induced PRL release is ERalpha dependent.

Indexed as

AnimalsCells, CulturedDose-Response Relationship, DrugEpidermal Growth FactorErbB ReceptorsEstrogen Receptor alphaEstrogen Receptor ModulatorsGene Expression RegulationLactotrophsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3PhosphorylationProlactinRatsTime FactorsEpidermal Growth FactorErbB ReceptorsEstrogen Receptor alphaEstrogen Receptor ModulatorsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Prolactin

Identifiers

PMID18832099
PMCPMC2646526
OpenAlexW2005896512

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.