ArticleFrontiers in immunology2026
Butyrate blocks cell cycle progression in colorectal cancer organoids partially through HDAC2 inhibition.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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.
Who cites it
1 citing paper in PubMed.
- Berberine restrains the expansion of colorectal cancer organoids by blocking cell cycle progression and reducing lipid synthesis.Frontiers in immunology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Butyric acid is a major gut microbiota metabolite that exhibits many biological functions, including the suppression of colorectal cancer (CRC) growth. However, previous studies have mainly been conducted using cell lines, which do not recapitulate the genuine three-dimensional spatial characteristics of CRC. In this study, we explored the therapeutic outcome and precise molecular targets of butyrate with sodium butyrate (NaB) using tumor organoids of CRC. Methods: Firstly, we examined the influence of butyrate on CRC subcutaneous allografts. And then the biological effects of butyrate were mainly determined using CRC organoids derived from KPC mice and Caco-2 cells. The morphological characteristics of butyrate-treated CRC organoids were analyzed, and multiple experimental assays were employed to determine the biological and molecular influences of butyrate. Finally, the inhibitor of HDAC2 was used to mimic the biological effects of butyrate on CRC organoids. Results: It was observed that butyrate significantly suppressed the growth of CRC allografts. Importantly, butyrate could apparently inhibit the proliferation, disrupt epithelial integrity, and induce apoptosis in CRC organoids. Transcriptomic analyses revealed that butyrate acts as an epigenetic modulator, targeting HDAC2 and selectively repressing its transcription. This led to inhibition of cyclin D1, CDK4/6, and upregulation of p21 expression, suggesting cell cycle arrest. The selective HDAC2 inhibitor similarly recapitulated the influences of butyrate on CRC organoids. Discussion: Butyrate exerts the definitive blocking effects on cell cycle progression in CRC organoids, and HDAC2 is one of the important targets. Butyrate modulates cell cycle via targeting HDAC2, constituting a novel therapeutic pathway for CRC. This study provides new evidence for gut microbial metabolites as a potential means for the prevention and treatment of colorectal cancer.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.