Evidence map›Paper›PMID 40195469›Full record

ArticleScientific reports2025

The butyrate derived from probiotic Clostridium butyricum exhibits an inhibitory effect on multiple myeloma through cell death induction.

Hiroaki Konishi, Takeshi Saito, Shuichiro Takahashi, Hiroki Tanaka, Katsuhiro Okuda, Hiroaki Akutsu, Tatsuya Dokoshi, Aki Sakatani, Keitaro Takahashi, Katsuyoshi Ando and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Gut microbes · 2026
    Article
  2. Review
  3. Oncology research · 2026
    Review
  4. Review
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.

Hiroaki KonishiDepartment of Gastroenterology and Advanced Medical Sciences, Asahikawa Medical University, 2-1-1-1, Midorigaoka-Higashi, Asahikawa, Hokkaido, 078-8510, Japan. hkonishi@asahikawa-med.ac.jp.
Takeshi SaitoDivision of Hematology, Department of Internal Medicine, Asahikawa Medical University, 2-1-1-1, Midorigaoka-Higashi, Asahikawa, Hokkaido, 078-8510, Japan.
Shuichiro TakahashiDivision of Hematology, Department of Internal Medicine, Asahikawa Medical University, 2-1-1-1, Midorigaoka-Higashi, Asahikawa, Hokkaido, 078-8510, Japan.
Hiroki TanakaDivision of Tumor Pathology, Department of Pathology, Asahikawa Medical University, 2-1 -1-1, Midorigaoka-Higashi, Asahikawa, Hokkaido, 078-8510, Japan.
Katsuhiro OkudaDepartment of Legal Medicine, Asahikawa Medical University, 2-1-1-1, Midorigaoka-Higashi, Asahikawa, Hokkaido, 078-8510, Japan.
Hiroaki AkutsuCentral Laboratory for Research and Education, Research Technology Support Center, Asahikawa Medical University, 2-1-1-1, Midorigaoka-Higashi, Asahikawa, Hokkaido, 078-8510, Japan.
Tatsuya DokoshiDivision of Gastroenterology, Department of Internal Medicine, Asahikawa Medical University, 2-1-1-1, Midorigaoka-Higashi, Asahikawa, Hokkaido, 078-8510, Japan.
Aki SakataniDepartment of Gastroenterological Sciences, Asahikawa Medical University, 2-1-1-1, Midorigaoka-Higashi, Asahikawa, Hokkaido, 078-8510, Japan.
Keitaro TakahashiDivision of Gastroenterology, Department of Internal Medicine, Asahikawa Medical University, 2-1-1-1, Midorigaoka-Higashi, Asahikawa, Hokkaido, 078-8510, Japan.
Katsuyoshi AndoDivision of Gastroenterology, Department of Internal Medicine, Asahikawa Medical University, 2-1-1-1, Midorigaoka-Higashi, Asahikawa, Hokkaido, 078-8510, Japan.
Shin KashimaDivision of Gastroenterology, Department of Internal Medicine, Asahikawa Medical University, 2-1-1-1, Midorigaoka-Higashi, Asahikawa, Hokkaido, 078-8510, Japan.
Nobuhiro UenoDepartment of Gastroenterological Sciences, Asahikawa Medical University, 2-1-1-1, Midorigaoka-Higashi, Asahikawa, Hokkaido, 078-8510, Japan.
Kentaro MoriichiDivision of Gastroenterology, Department of Internal Medicine, Asahikawa Medical University, 2-1-1-1, Midorigaoka-Higashi, Asahikawa, Hokkaido, 078-8510, Japan.
Naoki OgawaCentral Laboratory for Research and Education, Research Technology Support Center, Asahikawa Medical University, 2-1-1-1, Midorigaoka-Higashi, Asahikawa, Hokkaido, 078-8510, Japan.
Mikihiro FujiyaDepartment of Gastroenterology and Advanced Medical Sciences, Asahikawa Medical University, 2-1-1-1, Midorigaoka-Higashi, Asahikawa, Hokkaido, 078-8510, Japan.

Funding

Japan Society for the Promotion of Science 21K07929Japan Society for the Promotion of Science 21KK0291Japan Society for the Promotion of Science 22K08047
6 · The paper itself

Abstract

Multiple myeloma (MM) is a hematological malignancy characterized by a poor prognosis. While certain probiotics have been shown to produce antitumor molecules that inhibit solid tumor progression, it remains unclear whether probiotic-derived compounds can exert similar effects on hematological tumors, such as MM. In this study, we screened the cell-free culture supernatants (CFCS) of 24 probiotic strains for antitumor effects against multiple myeloma (MM) cells and identified that the CFCS from Clostridium butyricum (C. butyricum) demonstrated the most significant reduction in MM cell viability. Further fractionation of this CFCS through reverse-phase and gel filtration chromatography revealed a high enrichment of butyrate in the antitumor fraction, as confirmed by gas chromatography-mass spectrometry. Butyrate reduced MM cell viability in a concentration-dependent manner. Butyrate was significantly more cytotoxic to RPMI-8226 cells than peripheral blood mononuclear cells (PBMCs) isolated from two non-cancerous individuals. In the xenograft model of RPMI-8226 cells, butyrate showed significant inhibition of tumor formation. Cell cycle analysis showed that butyrate induced G1 phase arrest and increased sub-G1 phase, suggesting DNA fragmentation. Western blot analysis demonstrated that butyrate treatment led to cleaved poly ADP-ribose polymerase (PARP) accumulation. Additionally, flow cytometry showed an increase in annexin V positive MM cells, indicating apoptosis. Butyrate also exhibited synergistic antitumor activity when combined with bortezomib, a proteasome inhibitor. These findings suggest that probiotic-derived molecules, including butyrate, may enhance the therapeutic effect of hematological malignancy, such as MM.

Indexed as

Antineoplastic AgentsButyratesClostridium butyricumMultiple MyelomaProbioticsAnimalsApoptosisCell DeathCell Line, TumorCell SurvivalHumansMiceXenograft Model Antitumor AssaysAntineoplastic AgentsButyrates

Identifiers

PMID40195469
PMCPMC11976985

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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.