Evidence map›Paper›PMID 23518503›Full record

ArticleCell cycle (Georgetown, Tex.)2013

Interaction between p53 and estradiol pathways in transcriptional responses to chemotherapeutics.

Mattia Lion, Alessandra Bisio, Toma Tebaldi, Veronica De Sanctis, Daniel Menendez, Michael A Resnick, Yari Ciribilli, Alberto Inga

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.1field-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

29 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Novel Diagnostic Biomarkers in Colorectal Cancer.International journal of molecular sciences · 2022
    Review
  5. Article
  6. iScience · 2021
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Regulated large-scale nucleosome density patterns and precise nucleosome positioning correlate with V(D)J recombination.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  14. Article
  15. Article
  16. Article
  17. Article
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  19. Article
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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

8 authors at 3 institutions in 3 countries.

Mattia LionLaboratory of Transcriptional Networks, Centre for Integrative Biology (CIBIO), University of Trento, Mattarello, Trento, Italy.
Alessandra Bisio
Toma Tebaldi
Veronica De Sanctis
Daniel Menendez
Michael A Resnick
Yari Ciribilli
Alberto Inga
University of Trento · ITResearch Triangle Park Foundation · USGenomics (United Kingdom) · GB

Funding

Human Genes Affecting Chromosome Metabolism and Stress ResponseZIAES065079 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI MENENDEZ RENDON, DANIEL · 2009 to 2021
$12.5M
ISOLATION &CHARACTERIZATION OF GENES AFFECTING YEAST CHROMOSOME METABOLISMZ01ES065079 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI RESNICK, MICHAEL A · 1994 to 2008
$1.8M
Intramural NIH HHS Z01 ES065079
6 · The paper itself

Abstract

Estrogen receptors (ERs) and p53 can interact via cis-elements to regulate the angiogenesis-related VEGFR-1 (FLT1) gene, as we reported previously. Here, we address cooperation between these transcription factors on a global scale. Human breast adenocarcinoma MCF7 cells were exposed to single or combinatorial treatments with the chemotherapeutic agent doxorubicin and the ER ligand 17β-estradiol (E2). Whole-genome transcriptome changes were measured by expression microarrays. Nearly 200 differentially expressed genes were identified that showed limited responsiveness to either doxorubicin treatment or ER ligand alone but were upregulated in a greater than additive manner following combined treatment. Based on exposure to 5-fuorouracil and nutlin-3a, the combined responses were treatment-specific. Among 16 genes chosen for validation using quantitative real-time PCR, seven (INPP5D, TLR5, KRT15, EPHA2, GDNF, NOTCH1, SOX9) were confirmed to be novel direct targets of p53, based on responses in MCF7 cells silenced for p53 or cooperative targets of p53 and ER. Promoter pattern searches and chromatin IP experiments for the INPP5D, TLR5, KRT15 genes supported direct, cis-mediated p53 and/or ER regulation through canonical and noncanonical p53 and ER response elements. Collectively, we establish that combinatorial activation of p53 and ER can induce novel gene expression programs that have implications for cell-cell communications, adhesion, cell differentiation, development and inflammatory responses as well as cancer treatments.

Indexed as

Blotting, WesternDoxorubicinEstradiolFluorouracilGene Expression ProfilingGene Expression RegulationHumansImidazolesMCF-7 CellsMicroarray AnalysisPiperazinesReal-Time Polymerase Chain ReactionTime FactorsTranscription, GeneticTumor Suppressor Protein p53DoxorubicinEstradiolFluorouracilImidazolesnutlin 3PiperazinesTumor Suppressor Protein p5317-beta estradiolcis-elementdoxorubicinestrogen receptorMCF7 cellsnon-canonical response elementsnutlinp53synergistic cooperationsynergy

Identifiers

PMID23518503
PMCPMC3674086
OpenAlexW1970741995

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.