Evidence map›Paper›PMID 25616260›Full record

ArticleEnvironmental health perspectives2015

Effects of atrazine on estrogen receptor α- and G protein-coupled receptor 30-mediated signaling and proliferation in cancer cells and cancer-associated fibroblasts.

Lidia Albanito, Rosamaria Lappano, Antonio Madeo, Adele Chimento, Eric R Prossnitz, Anna Rita Cappello, Vincenza Dolce, Sergio Abonante, Vincenzo Pezzi, Marcello Maggiolini

Open access · diamondAbstract read
In one paragraph

Article in Environmental health perspectives, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
7.7field-weighted citation impact, top 2% 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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.

  1. A Review of Biomonitoring for Atrazine and Atrazine Metabolites Using Blood, Urine, and Sweat-Based Assays.International journal of environmental research and public health · 2026
    Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 2 countries.

Lidia AlbanitoDepartment of Pharmacy, Health and Nutritional Sciences, University of Calabria, Rende, Italy.
Rosamaria Lappano
Antonio Madeo
Adele Chimento
Eric R Prossnitz
Anna Rita Cappello
Vincenza Dolce
Sergio Abonante
Vincenzo Pezzi
Marcello Maggiolini
University of Calabria · ITUniversity of New Mexico · US

Funding

The Role of GPR30 in Advanced Endometrial CancerR01CA118743 · NCI · UNIVERSITY OF NEW MEXICO · PI PROSSNITZ, ERIC R · 2007 to 2009
$855k
NCI NIH HHS CA118743NCI NIH HHS R01 CA118743
6 · The paper itself

Abstract

backgroundThe pesticide atrazine does not bind to or activate the classical estrogen receptor (ER), but it up-regulates the aromatase activity in estrogen-sensitive tumor cells. The G protein estrogen receptor (GPR30/GPER) has been reported to be involved in certain biological responses to endogenous estrogens and environmental compounds exerting estrogen-like activity.

objectivesWe aimed to evaluate the potential of atrazine to trigger GPER-mediated signaling in cancer cells and cancer-associated fibroblasts (CAFs). METHODS AND

resultsUsing gene reporter assays in diverse types of cancer cells, we found that atrazine did not transactivate endogenous ERα or chimeric proteins that encode the ERα and ERβ hormone binding domains. Conversely, atrazine was able to bind to GPER to induce ERK activation and the expression of estrogen target genes, which, interestingly, appeared to rely on both GPER and ERα expression. As a biological counterpart, atrazine stimulated the proliferation of ovarian cancer cells that depend on GPER and ERα, as evidenced by gene silencing experiments and the use of specific signaling inhibitors. Of note, through GPER, atrazine elicited ERK phosphorylation, gene expression, and migration in CAFs, thus extending its stimulatory role to these main players of the tumor microenvironment.

conclusionsOur results suggest a novel mechanism through which atrazine may exert relevant biological effects in cancer cells and CAFs. On the basis of our data, atrazine should be included among the environmental contaminants that may elicit estrogenic activity through GPER-mediated signaling.

Indexed as

AtrazineCell Line, TumorCell MovementCell ProliferationEstrogen Receptor alphaFibroblastsHumansReceptors, G-Protein-CoupledSignal TransductionAtrazineEstrogen Receptor alphaReceptors, G-Protein-Coupled

Identifiers

PMID25616260
PMCPMC4421771
OpenAlexW2026198636

What OpenQuestion holds

Textmetadata
LicenceCC0
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.