Table 1 Summary of key bacterial genetic loci with potential links to the onset and development of cancer based on recent literature
Bacterial Species | Gene product | Mechanism of action | Potential associated cancer | References |
|---|---|---|---|---|
Helicobacter pylori | CagA | Dysregulation of Wnt/β catenin signalling cascade. Activation of NF-kB, leads to gastric inflammation and dysplasia | Gastric cancer | |
Helicobacter pylori | VacA and OipA | Induce gastric epithelial apoptosis which is associated with ulceration and aberrant cell proliferation in gastric tissue, leading to metaplasia and oncogenesis | Gastric cancer | [61] |
Fusobacterium nucleatum | FadA | Adheres to E-cadherin (a tumour suppressor) and stimulates Wnt/β catenin pathway. Inflammatory process leads to proliferation of colorectal cancer cells | Colorectal cancer | [62] |
Escherichia coli | Colibactin | DNase activity, creates double stranded breaks within epithelial cells. Promotes cell proliferation and tumour maturation | Colorectal cancer | |
Escherichia coli | Colibactin A (clbA) | clbA encodes a phosphopantetenyl transferase, subsequently modifying the three polypeptide synthases of the Pks locus | Colorectal cancer | [63] |
Colibactin P (clbP) | clbP codes for peptidase and splices a precursor of colibactin (pre-colibactin) into its active form | |||
Bacteroides fragilis | Bft | Stimulates colonic stat 3 activity and Th17 mucosal immune response. Cleaves E-cadherin, triggers β-catenin nuclear signalling. Linked to colon cell hyperplasia and cell proliferation | Colorectal cancer | |
Porphyromonas gingivalis | PPAD | Can instigate arginine degradation, which antagonises P53 gene and KRAS mutation | Pancreatic cancer | [65] |
Porphyromonas gingivalis | Gingipains | Promotes activation of MMP-9 proenzyme into its mature form leading to tumour cell proliferation | Oral cavity metastasis | [66] |