ArticleNature communications2026
Intermittent fasting inhibits Tp53-driven glioma through gut microbiota-mediated methionine-m
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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
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Who cites it
4 citing papers in PubMed.
- Unveiling the molecular mechanism of Qingwen Baidu decoction against dengue fever: an integrated study of bioinformatic analysis, machine learning and network pharmacology.Functional & integrative genomics · 2026Article
- scDeepAPA: a deep learning framework for single-cell alternative polyadenylation identification.Briefings in bioinformatics · 2026Article
- Nitrogen fertilizer pollution and infant brain/CNS cancer.Discover oncology · 2026Article
- Gut microbiota induces immune-related alterations in gene expression, RNA methylation, and metabolism in glioblastoma revealed by single-cell and spatial multi-omics.Frontiers in immunology · 2026Article
Corrections and comments
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Authors and funding
20 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intermittent fasting (IF) has emerged as a potential cancer treatment modality, although its tumor-suppressive effects are limited. Glioblastoma (GBM) can be classified into CDKN2A subtype and TP53 subtype. Here, we discover that the efficacy of IF is correlated with tumor subtypes of GBM. IF significantly inhibite GBM progression in mice with the Tp53 GBM model, whereas its inhibitory effect is not significant in the Cdkn2a GBM model. Multi-omics sequencing is performed in the IF-responsive Tp53 GBM mouse model, delineating a comprehensive molecular profiling of IF that including the spatial transcriptome, spatial metabolome, single-cell transcriptome, single-cell RNA methylation, metabolome, and microbiome. Through systematic biological analysis and rescue experiments conducted in IF-responsive Tp53 GBM mice model, we demonstrate that the efficacy of IF is primarily mediated by alterations in the gut microbiota, which subsequently modulate the production of the microbial metabolite methionine sulfoxide. Methionine sulfoxide, by regulating m
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Registered trials
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