Tier 4 — mechanistic

Inhibitory Effects of Apigenin on Tumor Carcinogenesis by Altering the Gut Microbiota

Shichang Bian, Hongjuan Wan, Xinyan Liao, Weisheng Wang
Mediators of Inflammation 2020 2020:7141970

Bibliography

PubMed
PMID 33082711
PubMed Central
PMC7559228
DOI
10.1155/2020/7141970
Funding
Supported by the National Natural Science Foundation of China (81600509) and the Tianjin Science and Technology Support Key Project Plan (20140109).
Competing interests
The authors declared no commercial or financial relationships that could be construed as a potential conflict of interest.

Study snapshot

DesignAOM/DSS colorectal-carcinogenesis mouse experiment with 16S sequencing, antibiotic microbiota depletion and fecal microbiota transplantation
ModelFour-week-old female specific-pathogen-free BALB/c mice
SampleKey experimental groups used n=8 mice per group.
InterventionDietary apigenin 30 mg/kg in tumor-bearing mice; antibiotic microbiota depletion; fecal microbiota transfer from apigenin-treated versus control donors.
DurationAOM/DSS induction over repeated 19-day cycles, with additional microbiota-depletion and fecal-transfer protocols.
EndpointsTumor number and size; Histological score; 16S gut microbiota composition; OTU and diversity measures; Effect after microbiota depletion; Transferability of antitumor effect by fecal microbiota

What the study showed, in plain terms

In a mouse model of inflammation-associated colon cancer, apigenin reduced tumor burden and changed the gut microbiota. When gut bacteria were depleted with antibiotics, the antitumor effect disappeared. Transferring fecal microbiota from apigenin-treated mice to other mice transferred part of the tumor-suppressive phenotype, supporting a microbiome-mediated mechanism in this animal model.

Key findings

Apigenin-treated mice developed fewer and smaller tumors. Gut microbial composition changed with treatment. Depleting the microbiota removed the apparent antitumor benefit, while fecal transfer from apigenin-treated donors inhibited tumor carcinogenesis in recipients.

What this study can and cannot tell us

This is an induced colorectal-cancer model in mice, not a human cancer trial. The exact microbial taxa and molecular mediators responsible for the effect were not fully established, and a 30 mg/kg mouse dietary exposure cannot be translated directly into a human supplement dose.

Editorial review

Reviewed by the Biohack Blueprint research team

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Dr. Khaled Mahmoud, MBBChCritical Care Medicine, Longevity Science & Editorial Direction Dr. Amr Yasser, PhDCardiometabolic, Musculoskeletal, Gut & Bioavailability Dr. Abdulla Mostafa, PhDCellular Senescence, Neurological, Mitochondrial & Brain-Ageing Biology