Gut microbial metabolite butyrate suppresses hepatocellular carcinoma growth via CXCL11-dependent enhancement of natural killer cell infiltration

Gut microbiota-derived butyrate plays a vital role in attenuating hepatocellular carcinoma (HCC) in murine models. However, the precise molecular mechanisms by which butyrate exerts its effects are largely undefined. Plasma short-chain fatty acids (SCFAs) were quantitatively measured by using gas chromatography-mass spectrometry (GC-MS) to access their association with HCC prognosis. Tumor-infiltrating immune cells were characterized by flow cytometry. The interactions between butyrate and natural killer (NK) cells were studied using in vitro assays, including migration, cytotoxic degranulation, and co-culture experiments. In vivo validation was conducted through neutralization experiments. The molecular pathways regulated by butyrate were further investigated by employing RNA sequencing (RNA-seq), chromatin immunoprecipitation sequencing (ChIP-seq), and Assay for Transposase-Accessible Chromatin using sequencing (ATAC-seq). A positive correlation was observed between elevated plasma butyrate levels and improved prognosis in HCC patients. Notably, butyrate inhibited tumor progression by enhancing NK cell infiltration into tumor tissues. Mechanistically, butyrate stimulated cytokine secretion, notably significantly enhancing the production of the chemokine CXCL11, thereby facilitating NK cell infiltration. Gene Set Enrichment Analysis (GSEA) of hepatic tumor cell lines revealed that the chemokine signaling and NK cell-mediated cytotoxicity pathways were upregulated following butyrate stimulation. Furthermore, transcriptomic and epigenomic analyses showed that exposure to butyrate induced de novo chromatin accessibility and enhancer remodeling, regulated by STAT family transcription factors. Our study demonstrated that butyrate was able to enhance the expression of CXCL11. This is likely attributed to chromatin remodeling, and then promoting NK cell infiltration and exerting effective anti-tumor effects on HCC.

Authors

Institutions

Publication Details

Journal
Gut Microbes
Published
2025-06-27
DOI
https://doi.org/10.1080/19490976.2025.2519706
Citations
17
Primary Topic
Gut microbiota and health
Type
article
Field-Weighted Citation Impact
13.70

Funders

Controls
|||
ALL TIME
JAN
FEB
MAR
APR
MAY
JUN
JUL
AUG
SEP
OCT
article

Gut microbial metabolite butyrate suppresses hepatocellular carcinoma growth via CXCL11-dependent enhancement of natural killer cell infiltration

Xuefeng Huang, Minghang Yu, Xiaoxue Yuan, Huichun Xing et al.
17 citations
Gut Microbes
Gut microbiota and health
13.70
article

Gut microbial metabolite butyrate suppresses hepatocellular carcinoma growth via CXCL11-dependent enhancement of natural killer cell infiltration

Xuefeng Huang, Minghang Yu, Xiaoxue Yuan, Huichun Xing, Xi Wang, Лей Ма, Yanlong Zhang, Changwen Zhang, Yifan Xu
article en
17 citations

Abstract

Gut microbiota-derived butyrate plays a vital role in attenuating hepatocellular carcinoma (HCC) in murine models. However, the precise molecular mechanisms by which butyrate exerts its effects are largely undefined. Plasma short-chain fatty acids (SCFAs) were quantitatively measured by using gas chromatography-mass spectrometry (GC-MS) to access their association with HCC prognosis. Tumor-infiltrating immune cells were characterized by flow cytometry. The interactions between butyrate and natural killer (NK) cells were studied using in vitro assays, including migration, cytotoxic degranulation, and co-culture experiments. In vivo validation was conducted through neutralization experiments. The molecular pathways regulated by butyrate were further investigated by employing RNA sequencing (RNA-seq), chromatin immunoprecipitation sequencing (ChIP-seq), and Assay for Transposase-Accessible Chromatin using sequencing (ATAC-seq). A positive correlation was observed between elevated plasma butyrate levels and improved prognosis in HCC patients. Notably, butyrate inhibited tumor progression by enhancing NK cell infiltration into tumor tissues. Mechanistically, butyrate stimulated cytokine secretion, notably significantly enhancing the production of the chemokine CXCL11, thereby facilitating NK cell infiltration. Gene Set Enrichment Analysis (GSEA) of hepatic tumor cell lines revealed that the chemokine signaling and NK cell-mediated cytotoxicity pathways were upregulated following butyrate stimulation. Furthermore, transcriptomic and epigenomic analyses showed that exposure to butyrate induced de novo chromatin accessibility and enhancer remodeling, regulated by STAT family transcription factors. Our study demonstrated that butyrate was able to enhance the expression of CXCL11. This is likely attributed to chromatin remodeling, and then promoting NK cell infiltration and exerting effective anti-tumor effects on HCC.

Gut MicrobesVol. 17(1)
King University (US), Capital University (US), Shanxi Medical University (CN), Capital Medical University (CN), Peking University (CN), National Institute for Communicable Disease Control and Prevention (CN), Institute for Forecasting of the Slovak Academy of Sciences (SK)
National Key Research and Development Program of China
Zero hunger
Openalex Percentile: Top 1%
Gut microbiota and health
13.70
AI Navigator

Ask Laika to Summarize, Analyze, and Connect papers live on the map.

Summarize Papers & Methodologies

Extract key findings, datasets, and comparative methods across publications.

Benchmark Rankings & Visual Analytics

Rank top research institutions, authors, funders, topics, and journals by Field-Weighted Citation Impact (FWCI) and paper volume with instant charts.

Connect Distant Disciplines

Bridge topological clusters on the map to find hidden collaborative intersections.