ArticleBreast cancer research : BCR2026
High-fat diet reshapes microbial interactions to promote breast cancer stemness via Streptococcus mutans-induced leucine accumulation.
Article in Breast cancer research : BCR, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
backgroundObesity and high-fat diet (HFD) are established risk factors for breast cancer, but the mechanisms by which dietary-induced gut microbiota alterations influence cancer progression are not fully understood. The interplay between microbial composition, metabolites, and cancer progression warrants further exploration.
methodsWe employed Mendelian randomization (MR) and Bayesian colocalization analyses based on genome-wide association studies (GWAS) to identify gut microbial genera causally linked to breast cancer risk. Multi-omics, including 16S rRNA sequencing, fecal metabolomics and RNA-seq, were performed to depict HFD-induced microbial and metabolic shifts in breast cancer-bearing mice. In vitro co-culture systems and in vivo murine models examined interactions between Roseburia intestinalis (R. intestinalis) and Streptococcus mutans (S. mutans) under HFD conditions. Functional assays, including immunofluorescence, qRT-PCR, probe-based assays and fluorescent in situ hybridization, and flow cytometry, evaluated cancer stemness, bacterial colonization, and the impact of leucine metabolism.
resultsMR analysis revealed Roseburia as a potential causal microbial risk factor for breast cancer, with colocalized genes enriched in fatty acid metabolism. HFD feeding promoted the co-occurrence of R. intestinalis and S. mutans, facilitating S. mutans intratumoral colonization and consequent leucine accumulation in the tumor microenvironment (TME). S. mutans-derived leucine robustly enhanced breast cancer cell proliferation and stemness, as evidenced by increased tumor sphere formation and upregulation of CD44, CD133, and SOX2. Functional blockade of leucine transport with BCH attenuated S. mutans-mediated tumor growth and limited tumor-associated macrophage activation in vivo.
conclusionsThis study reveals that HFD-induced reshaping of microbial interactions, particularly a commensal-like interaction between S. mutans and R. intestinalis, is associated with leucine accumulation in the TME, thereby supporting breast cancer stemness and progression. Targeting S. mutans-mediated leucine accumulation represents a promising strategy for therapeutic intervention in obesity-related breast cancer. Our findings highlight the pivotal role of dietary-microbiota crosstalk in modulating the TME and cancer stemness.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.