Evidence map›Paper›PMID 39523457›Full record

ArticleGut microbes

KRAS mutations promote the intratumoral colonization of enterotoxigenic bacteroides fragilis in colorectal cancer through the regulation of the miRNA3655/SURF6/IRF7/IFNβ axis.

Yizhen Chen, Shaolin Liu, Song Tan, Yuanyuan Zheng, Yifan Chen, Changshun Yang, Shengtao Lin, Yulong Mi, Weihua Li

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Gut microbes. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing 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

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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

23 citing papers in PubMed.

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  14. The role of CSTF2 in gastric cancer: implications for therapy.European journal of medical research · 2025
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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

9 authors.

Yizhen ChenShengli Clinical Medical College of Fujian Medical University, Fuzhou, China.
Shaolin LiuShengli Clinical Medical College of Fujian Medical University, Fuzhou, China.
Song TanShengli Clinical Medical College of Fujian Medical University, Fuzhou, China.
Yuanyuan ZhengShengli Clinical Medical College of Fujian Medical University, Fuzhou, China.
Yifan ChenShengli Clinical Medical College of Fujian Medical University, Fuzhou, China.
Changshun YangDepartment of Gastrointestinal Surgery, Fujian Provincial Hospital, Fuzhou University Affiliated Provincial Hospital, School of Medicine, Fuzhou University, Fuzhou, Fujian, China.
Shengtao LinDepartment of Gastrointestinal Surgery, Fujian Provincial Hospital, Fuzhou University Affiliated Provincial Hospital, School of Medicine, Fuzhou University, Fuzhou, Fujian, China.
Yulong MiDepartment of Gastrointestinal Surgery, Fujian Provincial Hospital, Fuzhou University Affiliated Provincial Hospital, School of Medicine, Fuzhou University, Fuzhou, Fujian, China.
Weihua LiDepartment of Gastrointestinal Surgery, Fujian Provincial Hospital, Fuzhou University Affiliated Provincial Hospital, School of Medicine, Fuzhou University, Fuzhou, Fujian, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

KRAS mutations are associated with poor prognosis in colorectal cancer (CRC). Although the association between the gut microbiota and CRC has been extensively documented, it is unclear whether KRAS mutations can regulate the gut microbiota. Metagenomics has identified changes in the diversity of the gut microbiota in CRC due to KRAS mutations. Specifically, KRAS mutations positively correlate with the abundance of the bacteroides. Understanding how to regulate the classic carcinogenic bacterium within the bacteroides, such as enterotoxigenic bacteroides fragilis (ETBF), to enhance treatment efficacy of tumors is a key focus of research. Mechanistically, we found that the reduction of miR3655 is indispensable for KRAS mutation-promoted proliferation of CRC and the abundance of ETBF. miR3655 targets SURF6 to inhibit its transcription. Further transcriptomic sequencing revealed that SURF6 promotes intratumoral colonization of ETBF in CRC by inhibiting the nuclear translocation and transcription levels of the IRF7, affecting the activation of the IFNβ promoter. Regulating miR3655 and SURF6 can promote IFNβ secretion in CRC, directly killing ETBF. These data indicate that KRAS mutations affect the intratumoral colonization of ETBF in CRC through the miR3655/SURF6/IRF7/IFNβ axis. This provides new potential strategies for treating CRC associated with KRAS mutations or high levels of ETBF.

Indexed as

Bacteroides fragilisColorectal NeoplasmsInterferon-betaInterferon Regulatory Factor-7MicroRNAsMutationProto-Oncogene Proteins p21(ras)AnimalsCell Line, TumorFemaleGastrointestinal MicrobiomeGene Expression Regulation, NeoplasticHumansMiceMice, NudeInterferon-betaInterferon Regulatory Factor-7KRAS protein, humanMicroRNAsProto-Oncogene Proteins p21(ras)colonizationColorectal cancerenterotoxigenic bacteroides fragilisintratumoural microbiotaKRAStumor microenvironment

Identifiers

PMID39523457
PMCPMC11556274

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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.