Evidence map›Paper›PMID 42091596›Full record

ArticleNPJ biofilms and microbiomes2026

Akkermansia muciniphila-derived 5-MIAA blunts colitis-associated tumorigenesis by modulating colonic SLC26A3/pSTAT3 signaling.

Binhai Shen, Hongbin Liu, Weifeng Huang, Ruo Huang, Qian Zhou, Xinlong Lin, Mengyao Song, Zheng Chen, Yin Zhang, Yinmu Li and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in NPJ biofilms and microbiomes, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. International journal of molecular sciences · 2026
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors.

Binhai Shen *Guangdong Provincial Key Laboratory of Gastroenterology, Institute of Gastroenterology of Guangdong Province, Department of Gastroenterology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Hongbin Liu *Guangdong Provincial Key Laboratory of Gastroenterology, Institute of Gastroenterology of Guangdong Province, Department of Gastroenterology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Weifeng Huang *Guangdong Provincial Key Laboratory of Gastroenterology, Institute of Gastroenterology of Guangdong Province, Department of Gastroenterology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Ruo HuangDepartment of Gastroenterology, The First People's Hospital of Foshan, Foshan, China.
Qian ZhouGuangdong Provincial Key Laboratory of Gastroenterology, Institute of Gastroenterology of Guangdong Province, Department of Gastroenterology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Xinlong LinGuangdong Provincial Key Laboratory of Gastroenterology, Institute of Gastroenterology of Guangdong Province, Department of Gastroenterology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Mengyao SongGuangdong Provincial Key Laboratory of Gastroenterology, Institute of Gastroenterology of Guangdong Province, Department of Gastroenterology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Zheng ChenGuangdong Provincial Key Laboratory of Gastroenterology, Institute of Gastroenterology of Guangdong Province, Department of Gastroenterology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Yin ZhangGuangdong Provincial Key Laboratory of Gastroenterology, Institute of Gastroenterology of Guangdong Province, Department of Gastroenterology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Yinmu LiGuangdong Provincial Key Laboratory of Gastroenterology, Institute of Gastroenterology of Guangdong Province, Department of Gastroenterology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Yandong GuoGuangdong Provincial Key Laboratory of Gastroenterology, Institute of Gastroenterology of Guangdong Province, Department of Gastroenterology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Lijun ZhengGuangzhou ZhiYi Biotechnology Co., Ltd, Guangzhou, China.
Yangyang LiuGuangzhou ZhiYi Biotechnology Co., Ltd, Guangzhou, China.
Fachao ZhiGuangdong Provincial Key Laboratory of Gastroenterology, Institute of Gastroenterology of Guangdong Province, Department of Gastroenterology, Nanfang Hospital, Southern Medical University, Guangzhou, China. zhifc41532@163.com.
Wendi ZhangGuangdong Provincial Key Laboratory of Gastroenterology, Institute of Gastroenterology of Guangdong Province, Department of Gastroenterology, Nanfang Hospital, Southern Medical University, Guangzhou, China. zhang_wendi@163.com.

Funding

Guangzhou Basic and Applied Basic Research Project 2025A04J3930National Natural Science Foundation of China 82172729National Natural Science Foundation of China 82373282Science and Technology Planning Project of Guangdong Province 2017B030314037
6 · The paper itself

Abstract

The interaction between gut microbiota and host genetic factors has been implicated in the development of colitis-associated colorectal cancer (CAC). Although Akkermansia muciniphila (Akk) has been studied in CAC, its role and molecular mechanism remain undetermined. In this study, we found that antibiotics treatment effectively inhibited tumorigenesis in azoxymethane/dextran sulfate sodium (AOM/DSS)-induced CAC mice, and was associated with an increase in Akk's relative abundance in feces. Akk supplementation, as well as its conditioned medium, remarkably restrained tumor formation in the CAC model, whereas the original medium did not yield the same results. Further untargeted metabolomics and germ-free mice experiments revealed that Akk generated a tryptophan metabolite 5-methoxyindole-3-acetic acid (5-MIAA), which demonstrated protective effects against CAC proliferation. Mechanistically, 5-MIAA boosted colonic SLC26A3 expression to suppress the phosphorylation of STAT3 (pSTAT3), thus inhibiting CAC proliferation, which was further validated by conditional knockout mice. Collectively, we revealed that a tryptophan metabolite 5-MIAA, derived from Akk, inhibited CAC proliferation through colonic SLC26A3/pSTAT3 signaling pathway, which indicated that Akk and its functional metabolites may serve as novel therapeutic approaches for the prevention and treatment of CAC.

Indexed as

AkkermansiaCarcinogenesisColitisColitis-Associated NeoplasmsIndoleacetic AcidsSTAT3 Transcription FactorSulfate TransportersAnimalsAnti-Bacterial AgentsAntiportersAzoxymethaneCell ProliferationColonDextran SulfateDisease Models, AnimalFecesAnti-Bacterial AgentsAntiportersAzoxymethaneDextran SulfateIndoleacetic AcidsSlc26a3 protein, mouseStat3 protein, mouseSTAT3 Transcription FactorSulfate Transporters

Identifiers

PMID42091596
PMCPMC13358060

What OpenQuestion holds

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Registered trials

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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.