# Gut bacterium metabolite fuels breast cancer in mice and organoids, Foshan team finds

- Published: 2026-11-07 03:16 UTC
- Section: Life & Health › Medicine
- Tags: Ruminococcus lactaris, UDP-GlcNAc, OGT enzyme, breast cancer progression, paclitaxel resistance, gut microbiota metabolite
- URL: https://realtech.media/news/rt-674797e2377b54ea046073d2_gut_bacterium_metabolite/

**Researchers showed that bacterial UDP-GlcNAc drives breast cancer progression via OGT signalling, while enzyme inhibition blocks tumor growth in preclinical models.**

![Gut bacterium metabolite fuels breast cancer in mice and organoids, Foshan team finds](https://realtech.media/media/2026/11/2892d7220550bf75.jpg)
*Syed Sajidul Islam, Wikimedia Commons, CC BY-SA 4.0*

A multidisciplinary research team led by Foshan Second People's Hospital and The First People's Hospital of Foshan / Southern University of Science and Technology has uncovered a direct signaling axis linking gut microbiota to breast cancer progression. Using multi-omics analysis of treatment-naïve patients, cell lines, mouse models, and patient-derived organoids, the scientists demonstrated that the commensal gut bacterium *Ruminococcus lactaris* produces uridine diphosphate N-acetylglucosamine (UDP-GlcNAc), a circulating oncometabolite that impairs chemotherapy response. The findings were published in 中国科学通报：英文版 [1].

## Microbial metabolite and host signaling circuit

Metagenomic and metabolomic analyses showed that *R. lactaris* was significantly enriched in patients with poor response to neoadjuvant chemotherapy. Although the host hexosamine biosynthetic pathway generates the majority of systemic UDP-GlcNAc, microbial de novo synthesis creates a critical shift that promotes tumor progression [1]. Once in the bloodstream, bacterial UDP-GlcNAc is absorbed by tumor cells and activates host O-GlcNAc transferase (OGT). This activation leads to the O-GlcNAcylation and stabilization of the transcription factor NFIB, which binds to the promoters of both OGT and the proto-oncogene KIT, establishing a self-amplifying feedback loop that drives cancer proliferation and migration [1].

## Chemotherapy resistance and enzyme inhibition

In both cell cultures and mouse models, systemic UDP-GlcNAc attenuated the anti-tumor efficacy of paclitaxel. Cancer cells exposed to paclitaxel alongside the microbial metabolite exhibited substantially higher viability compared to paclitaxel monotherapy [1]. Additionally, the team observed that *Streptomyces kanamyceticus* can convert UDP-GlcNAc into aminoglycoside antibiotics, which suppress Gram-negative competitors and foster an ecological niche favorable to *R. lactaris* expansion [1].

Pharmacological inhibition of OGT using the small-molecule inhibitor OSMI-1, as well as genetic silencing, completely disrupted this feed-forward signaling pathway in germ-free mice, specific-pathogen-free mice, and patient-derived breast cancer organoids. Tumor growth was suppressed despite the persistent presence of *R. lactaris* and elevated UDP-GlcNAc levels, confirming OGT as a viable molecular target to reverse bacteria-driven therapy resistance [1].

## Sources

1. [中国科学通报：英文版](https://doi.org/10.1016/j.scib.2026.10.022)
2. [EurekAlert](https://www.eurekalert.org/news-releases/1150820)

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Source: RealTech, realtech.media — https://realtech.media/news/rt-674797e2377b54ea046073d2_gut_bacterium_metabolite/