---
title: "Vitamin D limits mammary cancer bone invasion by reducing inflammation and EMT"
id: "biorxiv-0-vitamin-d-counters-bone-invasion-by-mammary-cancer-through-inhibition-of"
canonical_url: "https://medichelpline.com/clinical-feed/biorxiv-0-vitamin-d-counters-bone-invasion-by-mammary-cancer-through-inhibition-of"
content_type: "clinical_feed_article"
specialty: "Oncology"
source_name: "bioRxiv (Biomedical Preprints)"
source_url: "https://www.biorxiv.org/content/10.64898/2026.09.02.748895v1?rss=1"
published_at: "2026-09-03T12:00:00.000Z"
evidence_level: "Verified Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Vitamin D limits mammary cancer bone invasion by reducing inflammation and EMT
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/biorxiv-0-vitamin-d-counters-bone-invasion-by-mammary-cancer-through-inhibition-of
- **Specialty:** [Oncology](https://medichelpline.com/clinical-feed/oncology.md)
- **Primary Source:** bioRxiv (Biomedical Preprints)
- **Source URL:** [Original Journal Publication](https://www.biorxiv.org/content/10.64898/2026.09.02.748895v1?rss=1)
- **Published At:** 2026-09-03T12:00:00.000Z
- **Evidence Rating:** Verified Feed
## Executive GIST (TL;DR)
- This preprint reports that dietary vitamin D deficiency accelerates bone invasion by mammary cancer in a mouse model using tibial injection of MMTV-PyMT tumor cells in non-immunodeficient FVB mice. - The authors previously observed faster carcinogenesis and increased lung metastasis in vitamin D–deficient MMTV-PyMT mice; the present study focuses on mechanisms driving skeletal invasion. - Vitamin D deficiency was associated with increased pro‑inflammatory cytokines and higher **nestin** expression on internal bone surfaces and marrow, linking a pro‑inflammatory bone microenvironment to invasion. - The study identifies enhanced epithelial‑to‑mesenchymal transition (EMT) mediated via the transcription factor **Zeb1** in the vitamin D–deficient setting. - In vitro, the chemokine **CXCL12** induced Zeb1 expression in MMTV‑PyMT tumor cells; treatment with active vitamin D (1,25(OH)2D) countered this induction. - Treatment of tumor cells with 1,25(OH)2D reduced multiple pro‑inflammatory cytokines (GM‑CSF, ICAM‑1, IL‑1ra, IP‑10, JE, MCP‑5, MIP‑1α, MIP‑1β, MIP‑2, RANTES and CXCL12) in vitro. - Vitamin D repleteness correlated with very high expression of **Socs1**, a suppressor of cytokine signalling that inhibits JAK/STAT and limits excessive inflammatory responses and has tumor‑suppressive roles. - Authors propose that vitamin D sufficiency may reduce inflammation‑driven bone invasion and EMT, and suggest vitamin D repletion could enhance the efficacy of therapies aimed at preventing skeletal metastasis in breast cancer patients. - The article is a preprint and has not been peer reviewed; methodological details and full datasets are reported in the source but peer validation is pending.
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Jiarong Li Research Institute of the MUHC * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Jiarong%2BLi%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Li%20J&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AJiarong%2BLi%2B) Aimee-Lee Luco Research Institute of the MUHC * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Aimee-Lee%2BLuco%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Luco%20A&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AAimee-Lee%2BLuco%2B) Anne Camirand Research Institute of the MUHC * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Anne%2BCamirand%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Camirand%20A&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AAnne%2BCamirand%2B) Richard Kremer Research Institute of the MUHC * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Richard%2BKremer%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Kremer%20R&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3ARichard%2BKremer%2B) * For correspondence: richard.kremer@mcgill.ca * [Abstract](https://www.biorxiv.org/content/10.64898/2026.09.02.748895v1)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_art/node:5752959/1) * [Info/History](https://www.biorxiv.org/content/10.64898/2026.09.02.748895v1.article-info)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_info/node:5752959/1) * [Metrics](https://www.biorxiv.org/content/10.64898/2026.09.02.748895v1.article-metrics)[](https://www.biorxiv.org/panels_ajax_tab/article_tab_metrics/node:5752959/1) * [Supplementary material](https://www.biorxiv.org/content/10.64898/2026.09.02.748895v1.supplementary-material)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_data/node:5752959/1) * [ Preview PDF](https://www.biorxiv.org/content/10.64898/2026.09.02.748895v1.full.pdf+html)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_pdf/node:5752959/1) ![Loading](https://www.biorxiv.org/sites/all/modules/contrib/panels_ajax_tab/images/loading.gif) ## Abstract Vitamin D deficiency is associated with poor outcome in several cancers in humans, and administration of vitamin D or analogs has been shown to decrease tumor progression and metastasis in animal mammary cancer models. We previously demonstrated significant acceleration of carcinogenesis in vitamin D-deficient mouse mammary tumor virus-polyoma middle T (MMTV-PyMT) mammary cancer model as well as of its spontaneous metastasis to lungs. While vitamin D also plays a role in skeletal metastasis, detailed mechanisms of its promotion of bone invasion and metastatic events are not completely elucidated. In the present study we used tibially-injected MMTV-PyMT mammary tumor cells to analyse how dietary-induced vitamin D deficiency in non-immunodeficient FVB mice accelerates bone invasion. Mechanistically, we observed vitamin D deficiency to increase pro-inflammation cytokines and nestin expression in internal bone surface and marrow, and to increase epithelial-to-mesenchymal transition (EMT) through Zeb1 transcription factor. In vitro, treatment of MMTV-PyMT tumor cells with CXCL12 was observed to stimulate Zeb1 expression, and this effect was efficiently countered by 1,25(OH)2D treatment. Analysis of cytokines in MMTV-PyMT mammary tumor cells in vitro showed significant reduction in several pro-inflammatory cytokines with 1,25(OH)2D treatment (GM-CSF, ICAM-1, IL-1ra, IP-10, JE, MCP-5, MIP-1α, MIP-1β, MIP-2, RANTES and CXCL12), a crucial observation in view of the current evidence that inflammation is one of the hallmarks of cancer. Furthermore, vitamin D repleteness is associated with very high expression of Socs1 (suppressor of cytokine signalling 1), an inhibitor of JAK/STAT pathway which prevents excessive inflammatory responses and has a tumor-suppressive role. These findings provide a strong link between vitamin D deficiency and acceleration of inflammation-driven bone invasion, and nestin and EMT. The evidence suggests that vitamin D-repleteness in breast cancer patients could enhance the efficacy of co-administered therapies in preventing invasion of skeletal sites. ### Competing Interest Statement The authors have declared no competing interest. ## Funder Information Declared Canadian Institutes of Health Research, https://ror.org/01gavpb45, MOP 10839 Copyright The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a [CC-BY-NC-ND 4.0 International license](http://creativecommons.org/licenses/by-nc-nd/4.0/). 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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