Evidence map›Paper›PMID 31611907›Full record

ArticleFrontiers in genetics2019

Glyphosate Primes Mammary Cells for Tumorigenesis by Reprogramming the Epigenome in a TET3-Dependent Manner.

Manon Duforestel, Arulraj Nadaradjane, Gwenola Bougras-Cartron, Joséphine Briand, Christophe Olivier, Jean-Sébastien Frenel, François M Vallette, Sophie A Lelièvre, Pierre-François Cartron

Open access · goldAbstract read
In one paragraph

Article in Frontiers in genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

25 citing papers in PubMed, 61 citations in OpenAlex.

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  5. TET3 is expressed in prostate cancer tumor-associated macrophages and is associated with anti-androgen resistance.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
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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

9 authors at 4 institutions in 2 countries.

Manon DuforestelCRCINA, INSERM, Université de Nantes, Nantes, France.
Arulraj NadaradjaneCRCINA, INSERM, Université de Nantes, Nantes, France.
Gwenola Bougras-CartronCRCINA, INSERM, Université de Nantes, Nantes, France.
Joséphine BriandCRCINA, INSERM, Université de Nantes, Nantes, France.
Christophe OlivierCRCINA, INSERM, Université de Nantes, Nantes, France.
Jean-Sébastien FrenelCRCINA, INSERM, Université de Nantes, Nantes, France.
François M ValletteCRCINA, INSERM, Université de Nantes, Nantes, France.
Sophie A LelièvreDepartment of Basic Medical Sciences, Purdue University, West Lafayette, IN, United States.
Pierre-François CartronCRCINA, INSERM, Université de Nantes, Nantes, France.
Institut de Cancérologie de l'Ouest · FRCancéropôle Grand Ouest · FRCenter for Cancer Research · USNantes Université · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The acknowledgment that pollutants might influence the epigenome raises serious concerns regarding their long-term impact on the development of chronic diseases. The herbicide glyphosate has been scrutinized for an impact on cancer incidence, but reports demonstrate the difficulty of linking estimates of exposure and response analysis. An approach to better apprehend a potential risk impact for cancer is to follow a synergistic approach, as cancer rarely occurs in response to one risk factor. The known influence of glyphosate on estrogen-regulated pathway makes it a logical target of investigation in breast cancer research. We have used nonneoplastic MCF10A cells in a repeated glyphosate exposure pattern over 21 days. Glyphosate triggered a significant reduction in DNA methylation, as shown by the level of 5-methylcytosine DNA; however, in contrast to strong demethylating agent and cancer promoter UP peptide, glyphosate-treated cells did not lead to tumor development. Whereas UP acts through a DNMT1/PCNA/UHRF1 pathway, glyphosate triggered increased activity of ten-eleven translocation (TET)3. Combining glyphosate with enhanced expression of microRNA (miR) 182-5p associated with breast cancer induced tumor development in 50% of mice. Culture of primary cells from resected tumors revealed a luminal B (ER+/PR-/HER2-) phenotype in response to glyphosate-miR182-5p exposure with sensitivity to tamoxifen and invasive and migratory potentials. Tumor development could be prevented either by specifically inhibiting miR 182-5p or by treating glyphosate-miR 182-5p-cells with dimethyloxallyl glycine, an inhibitor of TET pathway. Looking for potential epigenetic marks of TET-mediated gene regulation under glyphosate exposure, we identified

Indexed as

breast cancerDNA methylationepigenetic markhypomethylationten-eleven translocation

Identifiers

PMID31611907
PMCPMC6777643
OpenAlexW2969860695

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.