Loading
Life sciences · Journal article
Frontiers in Cellular and Infection Microbiology · October 16, 2026
No summary has been generated for this record yet. What follows is drawn from its source metadata only.
Journal article.
No findings were extractable from the material analysed.
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
The source did not state who this applies to in practice.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
This record has not been graded across any dimension yet. Treat the label above as provisional and read the source.
What is missing. This record has no bottom line, key findings, reported figures, evidence dimensions. That is a gap in the analysis, not a judgement about the study.
Background Colorectal cancer (CRC) is a multifactorial disease driven by interactions among host genetics, immune dysregulation, environmental factors, and gut microbiota. The gut–tumor axis regulates CRC progression through inflammatory signaling, oxidative stress, epithelial barrier disruption, and immune imbalance. Probiotic-derived metabolites act as bioactive molecules capable of restoring host–microbiome homeostasis and modulating tumor-associated pathways. Objective To evaluate probiotic metabolites as adjunct therapeutic agents in CRC using integrative multi-omics analysis and in vitro validation. Methods A systems biology approach integrating network pharmacology, transcriptomics, proteomics, metabolomics, and microbiome profiling was applied. Twelve probiotic metabolites yielded 428 predicted targets, with 162 overlapping CRC-associated genes. CRC cell lines (HCT116, HT-29, Caco-2, SW480) were treated and analyzed for viability, apoptosis, gene/protein expression, cytokines, metabolites, and microbial composition. Results Sodium butyrate (5 mM) reduced cell viability by 35.5–42.3% (p < 0.001) and increased apoptosis from 8.6% to 32.4%, reaching 41.2% when combined with indole-3-acetic acid (IAA, 100 μM), suggesting a synergistic pro-apoptotic effect. RNA-seq identified 1,248 DEGs, with upregulation of BAX and CASP3 (log 2 FC +1.8 to +2.3) and downregulation of IL6, TNF, and NFKB1 (−1.5 to −2.1). Proteomics revealed 412 differentially expressed proteins, including downregulation of AKT1 (−1.6-fold), MAPK1 (−1.4-fold), and EGFR (−1.3-fold), and upregulation of CASP3 (+1.7-fold) and BAX (+1.5-fold). Cytokines IL-6, TNF-α, and IL-1β decreased by 48.2%, 44.7%, and 39.5%, respectively, while IL-10 increased by 26.3%. Metabolomics showed a 2.8-fold increase in butyrate and ~35% reduction in oxidative stress. Microbiome diversity improved (Shannon index 2.8–3.6). Conclusion Probiotic-derived metabolites modulate NF-κB, PI3K–Akt, MAPK, and apoptosis pathways, supporting their potential role as adjunct therapeutic agents in CRC management.