Fig. 1

The intricate interactions between the gut microbiota and cancer development. Deoxycholic acid and secondary BAs, such as fragilysin and FadA, contribute to DNA damage, SASP induction, and the upregulation of expression of oncogenic markers such as c-Myc and β-catenin, promoting carcinogenesis. Butyric acid, while generally exerting anti-inflammatory effects via GPR109a and p21, can also enhance inflammation through the AP-1 pathway. Additionally, bacterial toxins from H. pylori, P. aeruginosa, and Fusobacterium trigger activation of inflammatory pathways (NF-κB, AP-1) and genetic mutations (KRAS), leading to cancer development and metastasis. This depiction highlights the multifaceted role of the microbiota in carcinogenesis through various molecular mechanisms. Abbreviations: SASP: Senescence-associated secretory phenotype; FadA: Fusobacterium adhesin A; PCNA: Proliferating cell nuclear antigen; p21: Cyclin-dependent kinase tumour-suppressor protein inhibitor 1 A; AP-1: Activator protein-1; CagA: Cytotoxin-associated gene A; VacA: Vacuolating cytotoxin A; H. pylori: Helicobacter pylori