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Review
. 2023 Nov 30;4(1):45.
doi: 10.1186/s43556-023-00157-9.

Mechanisms by which the intestinal microbiota affects gastrointestinal tumours and therapeutic effects

Jikai He #  1 , Haijun Li #  2 , Jiaqi Jia  3 , Yang Liu  1 , Ning Zhang  1 , Rumeng Wang  1 , Wenhao Qu  3 , Yanqi Liu  4 , Lizhou Jia  5
Affiliations
Review

Mechanisms by which the intestinal microbiota affects gastrointestinal tumours and therapeutic effects

Jikai He et al. Mol Biomed. .

Abstract

The intestinal microbiota is considered to be a forgotten organ in human health and disease. It maintains intestinal homeostasis through various complex mechanisms. A significant body of research has demonstrated notable differences in the gut microbiota of patients with gastrointestinal tumours compared to healthy individuals. Furthermore, the dysregulation of gut microbiota, metabolites produced by gut bacteria, and related signal pathways can partially explain the mechanisms underlying the occurrence and development of gastrointestinal tumours. Therefore, this article summarizes the latest research progress on the gut microbiota and gastrointestinal tumours. Firstly, we provide an overview of the composition and function of the intestinal microbiota and discuss the mechanisms by which the intestinal flora directly or indirectly affects the occurrence and development of gastrointestinal tumours by regulating the immune system, producing bacterial toxins, secreting metabolites. Secondly, we present a detailed analysis of the differences of intestinal microbiota and its pathogenic mechanisms in colorectal cancer, gastric cancer, hepatocellular carcinoma, etc. Lastly, in terms of treatment strategies, we discuss the effects of the intestinal microbiota on the efficacy and toxic side effects of chemotherapy and immunotherapy and address the role of probiotics, prebiotics, FMT and antibiotic in the treatment of gastrointestinal tumours. In summary, this article provides a comprehensive review of the pathogenic mechanisms of and treatment strategies pertaining to the intestinal microbiota in patients with gastrointestinal tumours. And provide a more comprehensive and precise scientific basis for the development of microbiota-based treatments for gastrointestinal tumours and the prevention of such tumours.

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Conflict of interest statement

The authors declare that there are no conflicts of interest regarding the publication of this study.

Figures

Fig. 1
Fig. 1
Metabolite pathways. Abbreviations: LPS Lipopolysaccharides, TLR4 Toll-like receptor 4, FXR Farnesoid X receptor, DCA Deoxycholic acid, NFATc3 Nuclear factor of activated T cells 3, FOXP3 Forkhead box P3, GPCR G protein-coupled receptor, ERK Extracellular signal-regulated kinase, PI3K/Akt Phosphatidylinositol 3-kinase/Protein kinase B, IL Interleukin
Fig. 2
Fig. 2
Immune pathways. Abbreviations: LPS Lipopolysaccharides, PSA Polysaccharide A, TNF Tumour necrosis factor, NF-κB Nuclear factor-kappa B, FadA, Fusobacterium Nucleatum Adhesin A, BFT Bacteroides fragilis toxin, TLR2/4 Toll-like receptor 2/4, Treg Regulatory T cell, IL-10/17/6/22 Interleukin-10/17/6/22, Th17 Helper T cell 17, STAT3 Signal transduction and transcription factor 3, EMT Epithelial-mesenchymal transition, CTSK Cathepsin K, SAPK Stress-activated protein kinase, NO Nitric oxide, MDSC Myeloid-derived suppressor cell, NK Natural killer cell
Fig. 3
Fig. 3
Bacterial toxin pathways. Abbreviations: Cdt Cytolethal distending toxin, FadA Fusobacterium nucleatum adhesin A, BFT Bacteroides fragilis toxin, AvrA Avirulence protein A, STAT3 Signal transduction and transcription factor 3
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