---
title: "Alcohol Drives ER+ Breast Cancer Growth via Neuregulin‑1–Mediated ER–ErbB3 Signaling"
id: "biorxiv-0-alcohol-promotes-er-breast-cancer-cell-proliferation-and-invasion-through-the"
canonical_url: "https://medichelpline.com/clinical-feed/biorxiv-0-alcohol-promotes-er-breast-cancer-cell-proliferation-and-invasion-through-the"
content_type: "clinical_feed_article"
specialty: "Oncology"
source_name: "bioRxiv (Biomedical Preprints)"
source_url: "https://www.biorxiv.org/content/10.64898/2026.09.21.753250v1?rss=1"
published_at: "2026-09-22T12:00:00.000Z"
evidence_level: "Verified Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Alcohol Drives ER+ Breast Cancer Growth via Neuregulin‑1–Mediated ER–ErbB3 Signaling
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/biorxiv-0-alcohol-promotes-er-breast-cancer-cell-proliferation-and-invasion-through-the
- **Specialty:** [Oncology](https://medichelpline.com/clinical-feed/oncology.md)
- **Primary Source:** bioRxiv (Biomedical Preprints)
- **Source URL:** [Original Journal Publication](https://www.biorxiv.org/content/10.64898/2026.09.21.753250v1?rss=1)
- **Published At:** 2026-09-22T12:00:00.000Z
- **Evidence Rating:** Verified Feed
## Executive GIST (TL;DR)
- Alcohol exposure promotes proliferation, clonogenic growth, and S-phase progression in estrogen receptor–positive (**ER+**) breast cancer cell lines MCF-7 and T47D under estrogen‑depleted conditions. - Alcohol increases **ERα** phosphorylation and transcriptional activity, including greater ERα occupancy at the endogenous TFF1/pS2 regulatory region. - Alcohol activates the receptor tyrosine kinase **ErbB3** and downstream signaling pathways Akt, **ERK**, and p38. - Alcohol induces expression of **neuregulin‑1 (NRG1)** in both ER+ cell lines. - Pharmacologic blockade of ER signaling with ICI 182,780 (fulvestrant) substantially reduces alcohol-driven **NRG1** induction, ErbB3/RTK activation, and alcohol‑promoted growth, indicating dependence on functional ER signaling. - shRNA-mediated depletion of **NRG1** suppresses alcohol‑induced proliferation, clonogenicity, and cell‑cycle progression, and markedly reduces alcohol‑stimulated migratory and invasive phenotypes. - NRG1 depletion also attenuates ErbB3/Akt/ERK signaling and reduces ERα activation and estrogen‑response‑element (ERE)–dependent transcription, implying reciprocal reinforcement between ER activity and NRG1‑ErbB3 signaling. - The authors propose an **ER–NRG1–ErbB3** reciprocal signaling circuit in which alcohol‑induced ER activity drives NRG1 expression and NRG1‑dependent ErbB3 signaling sustains ER activation and tumor‑promoting phenotypes. - The study identifies **NRG1** as a molecular link between the estrogenic effects of alcohol and growth factor receptor signaling in ER+ breast cancer. - This work is reported as a preprint (not peer reviewed). Funding sources and a competing interest statement (no competing interests declared) are listed in the source.
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Zhikun Ma North Carolina Central University * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Zhikun%2BMa%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Ma%20Z&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AZhikun%2BMa%2B) Amanda B Parris North Carolina Central University * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Amanda%2BB%2BParris%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Parris%20AB&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AAmanda%2BB%2BParris%2B) Xiaohe Yang North Carolina Central University * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Xiaohe%2BYang%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Yang%20X&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AXiaohe%2BYang%2B) * For correspondence: xyang@nccu.edu * [Abstract](https://www.biorxiv.org/content/10.64898/2026.09.21.753250v1)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_art/node:5801910/1) * [Info/History](https://www.biorxiv.org/content/10.64898/2026.09.21.753250v1.article-info)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_info/node:5801910/1) * [Metrics](https://www.biorxiv.org/content/10.64898/2026.09.21.753250v1.article-metrics)[](https://www.biorxiv.org/panels_ajax_tab/article_tab_metrics/node:5801910/1) * [ Preview PDF](https://www.biorxiv.org/content/10.64898/2026.09.21.753250v1.full.pdf+html)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_pdf/node:5801910/1) ![Loading](https://www.biorxiv.org/sites/all/modules/contrib/panels_ajax_tab/images/loading.gif) ## Abstract Alcohol consumption is an established risk factor for breast cancer, with a particularly strong association with estrogen receptor-positive (ER+) disease. Although the estrogenic activity of alcohol is well recognized, how alcohol-induced ER signaling is coupled to growth factor receptor pathways that promote tumor cell growth and progression remains incompletely understood. Here, we identify neuregulin-1 (NRG1) as a functional mediator, linking alcohol-induced ER activity to ErbB3 receptor tyrosine kinase signaling in ER+ breast cancer cells. Under estrogen-depleted conditions, alcohol induced proliferation, clonogenic growth, and S-phase progression in MCF-7 and T47D cells. Alcohol concurrently increased ERα phosphorylation and transcriptional activity, including enhanced ERα occupancy at the endogenous TFF1/pS2 regulatory region, and activated ErbB3 and downstream Akt, ERK, and p38 signaling. Notably, alcohol induced NRG1 expression in both cell lines. Pharmacological inhibition of ER signaling with ICI 182,780 (fulvestrant) substantially attenuated NRG1 induction, ErbB3/RTK activation, and alcohol-promoted growth, indicating that NRG1 induction and engagement of RTK signaling are strongly dependent on functional ER signaling. Conversely, shRNA-mediated NRG1 depletion suppressed alcohol-induced proliferation, clonogenic growth, and cell-cycle progression and markedly reduced alcohol-induced migratory and invasive phenotypes. NRG1 depletion also attenuated ErbB3/Akt/ERK signaling while reducing ERα activation and ERE-dependent transcription, demonstrating a functional contribution of NRG1 to both arms of the signaling response. Together, these findings support a reciprocal ER-NRG1-ErbB3 signaling circuit in which alcohol-induced ER activity promotes NRG1 expression, while NRG1-dependent ErbB3 signaling reinforces ER activity and tumor-promoting phenotypes. Our study identifies NRG1 as a previously unrecognized molecular link between the estrogenic activity of alcohol and growth factor receptor signaling and provides a mechanistic framework for understanding alcohol-associated promotion of ER+ breast cancer. ### Competing Interest Statement The authors have declared no competing interest. ## Funder Information Declared National Institute of General Medical Sciences, 1R16GM145545 National Institute on Alcohol Abuse and Alcoholism, U54 AA019765 National Institute on Minority Health and Health Disparities, U54 MD012392 Copyright The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. All rights reserved. No reuse allowed without permission. bioRxiv and medRxiv thank the following for their generous financial support: > The Chan Zuckerberg Initiative, Cold Spring Harbor Laboratory, the Sergey Brin Family Foundation, California Institute of Technology, Centre National de la Recherche Scientifique, Fred Hutchinson Cancer Center, Imperial College London, Massachusetts Institute of Technology, Stanford University, The University of Edinburgh, University of Washington, and Vrije Universiteit Amsterdam. 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