# Glyphosate as an Emerging Environmental Pollutant and Its Effects on Breast Cancer Cell Proliferation: A Systematic Literature Review of Preclinical Evidence

**Authors:** Mario A. Alcalá-Pérez, Gustavo A. Hernández-Fuentes, Idalia Garza-Veloz, Uriel Diaz-Llerenas, Margarita L. Martinez-Fierro, José Guzmán-Esquivel, Fabian Rojas-Larios, Ángel A. Ramos-Organillo, Kayim Pineda-Urbina, José M. Flores-Álvarez, Juan P. Mojica-Sánchez, Jorge A. Cárdenas-Magaña, Cesar A. Villa-Martínez, Iván Delgado-Enciso

PMC · DOI: 10.3390/toxics14010026 · Toxics · 2025-12-26

## TL;DR

This review examines how glyphosate and glyphosate-based herbicides may affect breast cancer cell growth in lab studies, finding weak estrogenic effects but limited evidence overall.

## Contribution

The paper systematically reviews preclinical evidence on glyphosate's effects on breast cancer cells, highlighting its potential as a weak endocrine disruptor.

## Key findings

- Glyphosate exposure showed weak estrogenic activity in ER-positive breast cancer cells via ERα modulation.
- GBHs had greater cytotoxic and epigenetic effects in non-tumorigenic cells, often unrelated to estrogen receptor signaling.
- No in vivo breast cancer models were included in the reviewed studies.

## Abstract

The widespread use of glyphosate-based herbicides (GBHs) has raised concerns about their potential role in hormone-sensitive cancers such as breast cancer. This systematic review aimed to evaluate preclinical evidence on the effects of glyphosate (pure compound) or glyphosate-based herbicide formulations (GBHs) exposure on breast cancer cell proliferation and related molecular pathways. A structured search was conducted across PubMed, ScienceDirect, and Springer Nature Link, Web of Science databases, covering studies published up to 9 November 2025, following a PROSPERO-registered protocol (ID: CRD42021238350). Eligible studies included original in vitro and in vivo preclinical research using human breast cancer cell lines (e.g., MCF-7, T47D, MDA-MB-231, MCF-12A, and MCF-10A) or relevant animal models. Outcomes assessed included cell viability, proliferation, tumor growth, apoptosis, cell cycle regulation, and molecular markers associated with endocrine signaling. Two reviewers independently screened and extracted data, resolving disagreements via discussion or third-party adjudication. From an initial pool of 699 articles, seven in vitro studies met the inclusion and quality criteria. Glyphosate exposure demonstrated weak estrogenic activity in ER-positive breast cancer cells, primarily via ERα modulation and altered gene expression related to proliferation and DNA repair. GBHs showed greater cytotoxic and epigenetic effects in non-tumorigenic cells, often independent of ER signaling. No included study employed in vivo breast cancer models. Overall, preclinical evidence suggests glyphosate may act as a weak endocrine disruptor under specific conditions, but findings are limited by the short-term in vitro designs, heterogeneous methodologies, and lack of chronic or in vivo data. Further research using long-term exposure and animal models is needed to clarify potential risks and inform regulatory and public health decisions.

## Linked entities

- **Genes:** ESR1 (estrogen receptor 1) [NCBI Gene 2099]
- **Chemicals:** glyphosate (PubChem CID 3496)
- **Diseases:** breast cancer (MONDO:0004989)

## Full-text entities

- **Genes:** ESR1 (estrogen receptor 1) [NCBI Gene 2099] {aka ER, ESR, ESRA, ESTRR, Era, NR3A1}, EREG (epiregulin) [NCBI Gene 2069] {aka EPR, ER, Ep}
- **Diseases:** Breast Cancer (MESH:D001943), hormone-sensitive cancers (MESH:D009369), tumorigenic (MESH:D002471), cytotoxic (MESH:D064420), endocrine disruptor (MESH:D004700)
- **Chemicals:** glyphosate-based herbicides (-), Glyphosate (MESH:C010974)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12846237/full.md

## References

71 references — full list in the complete paper: https://tomesphere.com/paper/PMC12846237/full.md

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Source: https://tomesphere.com/paper/PMC12846237