Evidence map›Paper›PMID 21738574›Full record

ArticlePloS one2011

Proteomic analysis of pathways involved in estrogen-induced growth and apoptosis of breast cancer cells.

Zhang-Zhi Hu, Benjamin L Kagan, Eric A Ariazi, Dean S Rosenthal, Lihua Zhang, Jordan V Li, Hongzhan Huang, Cathy Wu, V Craig Jordan, Anna T Riegel and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
5.0field-weighted citation impact, top 5% 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

18 citing papers in PubMed, 36 citations in OpenAlex.

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  13. Modeling of the growth kinetics of occult breast tumors: role in interpretation of studies of prevention and menopausal hormone therapy.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2012
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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

11 authors at 3 institutions in 1 country.

Zhang-Zhi HuLombardi Cancer Center, Georgetown University, Washington, DC, United States of America.
Benjamin L Kagan
Eric A Ariazi
Dean S Rosenthal
Lihua Zhang
Jordan V Li
Hongzhan Huang
Cathy Wu
V Craig Jordan
Anna T Riegel
Anton Wellstein
Georgetown University · USGeorgetown University Medical Center · USFox Chase Cancer Center · US

Funding

Tissue Culture Shared ResourceP30CA051008 · NCI · GEORGETOWN UNIVERSITY · PI STEPHEN W BYERS · 1990 to 2026
$71.5M
SPORE IN BREAST CANCERP50CA058185 · NCI · GEORGETOWN UNIVERSITY · PI DICKSON, ROBERT B. · 1992 to 2004
$4.0M
Role of AIB1 in malignant progressionR01CA113477 · NCI · GEORGETOWN UNIVERSITY · PI RIEGEL, ANNA TATE · 2005 to 2015
$2.9M
NCI NIH HHS P30 CA051008NCI NIH HHS P50 CA058185NCI NIH HHS R01 CA113477
6 · The paper itself

Abstract

backgroundEstrogen is a known growth promoter for estrogen receptor (ER)-positive breast cancer cells. Paradoxically, in breast cancer cells that have been chronically deprived of estrogen stimulation, re-introduction of the hormone can induce apoptosis. METHODOLOGY/PRINCIPAL

findingsHere, we sought to identify signaling networks that are triggered by estradiol (E2) in isogenic MCF-7 breast cancer cells that undergo apoptosis (MCF-7:5C) versus cells that proliferate upon exposure to E2 (MCF-7). The nuclear receptor co-activator AIB1 (Amplified in Breast Cancer-1) is known to be rate-limiting for E2-induced cell survival responses in MCF-7 cells and was found here to also be required for the induction of apoptosis by E2 in the MCF-7:5C cells. Proteins that interact with AIB1 as well as complexes that contain tyrosine phosphorylated proteins were isolated by immunoprecipitation and identified by mass spectrometry (MS) at baseline and after a brief exposure to E2 for two hours. Bioinformatic network analyses of the identified protein interactions were then used to analyze E2 signaling pathways that trigger apoptosis versus survival. Comparison of MS data with a computationally-predicted AIB1 interaction network showed that 26 proteins identified in this study are within this network, and are involved in signal transduction, transcription, cell cycle regulation and protein degradation.

conclusionsG-protein-coupled receptors, PI3 kinase, Wnt and Notch signaling pathways were most strongly associated with E2-induced proliferation or apoptosis and are integrated here into a global AIB1 signaling network that controls qualitatively distinct responses to estrogen.

Indexed as

ApoptosisBreast NeoplasmsEstradiolFemaleHumansImmunoprecipitationMass SpectrometryNuclear Receptor Coactivator 3Phosphatidylinositol 3-KinasesProtein BindingProteomicsReceptors, G-Protein-CoupledReceptors, NotchSignal TransductionTumor Cells, CulturedWnt ProteinsEstradiolNCOA3 protein, humanNuclear Receptor Coactivator 3Phosphatidylinositol 3-KinasesReceptors, G-Protein-CoupledReceptors, NotchWnt Proteins

Identifiers

PMID21738574
PMCPMC3124472
OpenAlexW2014896281

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.