Fig. 1. Microbiota members associated with cancer risk at different body sites.
a) Microbiota members from the oropharyngeal, gastrointestinal, and genitourinary regions are implicated in cancer development and progression. Specifically, Fusobacterium nucleatum, Porphyromonas gingivalis, Escherichia coli, Helicobacter pylori, and Lactobacillus spp. are recognized bacterial risk factors for cancer. F. nucleatum can contribute to cancer development by inhibiting immune cell activity and activating tumorigenic pathways through outer membrane adhesins, Fap2 and FadA29. Further, F. nucleatum is known to translocate widely throughout the body, leading to its carcinogenic effects beyond the oral microbiome, including colorectal cancer185. P. gingivalis is equipped to inhibit cancer cell apoptosis through the activation of host signalling pathways, the expression of microRNAs, the secretion of nucleoside diphosphate kinases, and the inhibition of tumour suppressor p5329. P. gingivalis infection can activate various inflammatory pathways that induce the expression of pro-matrix metalloproteinase-9 (MMP-9)29, which is activated by P. gingivalis-secreted gingipains, leading to increased cell invasion, migration, and metastatic growth29. Enhanced P. gingivalis abundance has been observed in pancreatic, gingival, oesophageal, and colorectal cancer studies28,29,186–190. Lactobacillus spp. help maintain reproduction health, but the role of each species varies191. Reduced numbers of Lactobacillus species have been observed in samples of patients with urinary, ovarian, gastric, colorectal, and breast cancer192–195. Due to a decrease in lactic acid production, the pH shifts and creates a less hostile colonization niche for non-Lactobacillus species, enhancing susceptibility to infection. Lactobacilllus crispatus and Lactobacillus jensenii exhibit a reductive trend in cervical cancer while Lactobacillus iners enrichment is associated with a possible detrimental role30,196. H. pylori and E. coli are well-known contributors to gastric and colorectal cancer, respectively. b) Metabolites with links to cancer development include reactive oxygen and nitrogen species like hydrogen peroxide (contributes to sperminal), (geno)toxins like tilimycin, tilivalline and colibactin, and indole-functionalized metabolites including ʟ-tryptophan and indolimines.