Evidence map›Paper›PMID 21882221›Full record

ArticleJournal of cellular biochemistry2012

Forkhead box A1 (FOXA1) is a key mediator of insulin-like growth factor I (IGF-I) activity.

Adam S Potter, Angelo J Casa, Adrian V Lee

Open access · greenAbstract read
In one paragraph

Article in Journal of cellular biochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

17 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Review
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  6. Virus-like nanoparticles as a theranostic platform for cancer.Frontiers in bioengineering and biotechnology · 2022
    Review
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  8. Article
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  14. Review
  15. Pioneer factors in hormone-dependent cancers.Nature reviews. Cancer · 2012
    Review
  16. Article
  17. Article
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

3 authors at 1 institution in 1 country.

Adam S PotterLester and Sue Smith Breast Center, Baylor College of Medicine, Houston, Texas 77030, USA.
Angelo J Casa
Adrian V Lee
Baylor College of Medicine · US

Funding

Tumor BiologyP30CA125123 · NCI · BAYLOR COLLEGE OF MEDICINE · PI DAVID R ROWLEY · 2007 to 2026
$73.9M
TUMOR SUPPRESSOR GENES IN BREAST CANCER DEVELOPMENTP50CA058183 · NCI · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI OSBORNE, C KENT · 1992 to 2012
$30.9M
IRS1 and 2 Signaling in Mammary Development and CancerR01CA094118 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI LEE, ADRIAN V · 2002 to 2015
$3.0M
TRAINING PROGRAM IN MOLECULAR ENDOCRINOLOGYT32DK007696 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI MOORE, DAVID D · 1993 to 2012
$2.8M
NCI NIH HHS P30 CA125123NCI NIH HHS P50 CA058183NCI NIH HHS P50CA58183NCI NIH HHS R01 CA094118NCI NIH HHS R01CA94118NIDDK NIH HHS DK07696NIDDK NIH HHS T32 DK007696
6 · The paper itself

Abstract

The insulin-like growth factor receptor (IGF-IR) has been implicated in a number of human tumors, including breast cancer. Data from human breast tumors has demonstrated that IGF-IR is over-expressed and hyper-phosphorylated. Additionally, microarray analysis has shown that IGF-I treatment of MCF7 cells leads to a gene signature comprised of induced and repressed genes, which correlated with luminal B tumors. FOXA1, a forkhead family transcription factor, has been shown to be crucial for mammary ductal morphogenesis, similar to IGF-IR, and expressed at high levels in luminal subtype B breast tumors. Here, we investigated the relationship between FOXA1 and IGF-I action in breast cancer cells. We show that genes regulated by IGF-I are enriched for FOXA1 binding sites, and knock down of FOXA1 blocked the ability of IGF-I to regulate gene expression. IGF-I treatment of MCF7 cells increased the half-life of FOXA1 protein and this increase in half-life appeared to be dependent on canonical IGF-I signal transduction through both MAPK and AKT pathways. Finally, knock down of FOXA1 led to a decreased ability of IGF-I to induce proliferation and protect against apoptosis. Together, these results demonstrate that IGF-I can increase the stability of FOXA1 protein expression and place it as a critical mediator of IGF-I regulation of gene expression and IGF-I-mediated biological responses.

Indexed as

ApoptosisBinding SitesBreast NeoplasmsCell Line, TumorCell ProliferationFemaleGene Expression RegulationHepatocyte Nuclear Factor 3-alphaHumansInsulin-Like Growth Factor IMitogen-Activated Protein KinasesPhosphatidylinositol 3-KinaseRNA InterferenceRNA, Small InterferingSignal TransductionFOXA1 protein, humanHepatocyte Nuclear Factor 3-alphaInsulin-Like Growth Factor IMitogen-Activated Protein KinasesPhosphatidylinositol 3-KinaseRNA, Small Interfering

Identifiers

PMID21882221
PMCPMC3867524
OpenAlexW2146329585

What OpenQuestion holds

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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.