Evidence map›Paper›PMID 37261698›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2023

Clostridium butyricum and its metabolite butyrate promote ferroptosis susceptibility in pancreatic ductal adenocarcinoma.

Xiaotong Yang, Zhengyan Zhang, Xuqing Shen, Junyi Xu, Yawen Weng, Wei Wang, Jing Xue

Abstract read
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
9.7field-weighted citation impact, top 2% of its field
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

32 citing papers in PubMed, 42 citations in OpenAlex.

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  11. Ginsenoside Rh4 Triggers Ferroptosis in Lung Cancer: TargetingInternational journal of molecular sciences · 2026
    Article
  12. Microbiota in cancer: current understandings and future perspectives.Signal transduction and targeted therapy · 2026
    Review
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  17. Recent advances in the positive role ofFrontiers in immunology · 2026
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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

7 authors at 2 institutions in 1 country.

Xiaotong Yang *State Key Laboratory of Systems Medicine for Cancer , Stem Cell Research Center, Ren Ji Hospital, Shanghai Cancer Institute, Shanghai Jiao Tong University School of Medicine, 160 Pujian Rd, Shanghai, 200127, China.
Zhengyan Zhang *State Key Laboratory of Systems Medicine for Cancer , Stem Cell Research Center, Ren Ji Hospital, Shanghai Cancer Institute, Shanghai Jiao Tong University School of Medicine, 160 Pujian Rd, Shanghai, 200127, China.
Xuqing ShenState Key Laboratory of Systems Medicine for Cancer , Stem Cell Research Center, Ren Ji Hospital, Shanghai Cancer Institute, Shanghai Jiao Tong University School of Medicine, 160 Pujian Rd, Shanghai, 200127, China.
Junyi XuState Key Laboratory of Systems Medicine for Cancer , Stem Cell Research Center, Ren Ji Hospital, Shanghai Cancer Institute, Shanghai Jiao Tong University School of Medicine, 160 Pujian Rd, Shanghai, 200127, China.
Yawen WengState Key Laboratory of Systems Medicine for Cancer , Stem Cell Research Center, Ren Ji Hospital, Shanghai Cancer Institute, Shanghai Jiao Tong University School of Medicine, 160 Pujian Rd, Shanghai, 200127, China.
Wei WangDepartment of Gastroenterology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, No 100, Haining Road, Shanghai, 200080, China. wangwei_0306@163.com.
Jing XueState Key Laboratory of Systems Medicine for Cancer , Stem Cell Research Center, Ren Ji Hospital, Shanghai Cancer Institute, Shanghai Jiao Tong University School of Medicine, 160 Pujian Rd, Shanghai, 200127, China. jingxue@sjtu.edu.cn.
Shanghai Jiao Tong University · CNShanghai Cancer Institute · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposePancreatic ductal adenocarcinoma (PDAC) is a highly aggressive disease with limited therapeutic options. The diversity and composition of the intratumoral microbiota are associated with PDAC outcomes, and modulating the tumor microbiota has the potential to influence tumor growth and the host immune response. Here, we explore whether intervention with butyrate-producing probiotics can limit PDAC progression.

methodsBased on the TCGA (PAAD) database, we analyzed the differential communities of intratumoral microbiota in PDAC patients with long survival and short survival and explored the relevant mechanisms of Clostridium butyricum and its metabolite butyrate in the treatment of PDAC. Treatment with Clostridium butyricum or butyrate in combination with the ferroptosis inducer RSL3 in a PDAC mouse model has an inhibitory effect on PDAC progression. The potential molecular mechanisms were verified by flow cytometry, RNA-seq, Western blotting, qRT‒PCR and immunofluorescence.

resultsWe found that the tumoral butyrate-producing microbiota was linked to a better prognosis and less aggressive features of PDAC. Intervention with Clostridium butyricum or its metabolite butyrate triggered superoxidative stress and intracellular lipid accumulation, which enhanced ferroptosis susceptibility in PDAC.

conclusionOur study reveals a novel antitumor mechanism of butyrate and suggests the therapeutic potential of butyrate-producing probiotics in PDAC.

Indexed as

Carcinoma, Pancreatic DuctalClostridium butyricumFerroptosisPancreatic NeoplasmsAnimalsButyratesHumansMiceButyratesButyrateClostridium butyricumFerroptosisIntratumoral microbiotaPDAC

Identifiers

PMID37261698
PMCPMC12974734
OpenAlexW4378951980

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.