Table 1.
Bacteria involved in colorectal carcinogenesis.
| Effect pro-tumor/relation with cancer | References | |
|---|---|---|
| Streptococus gallolyticus | Expresses a collagen binding protein pil1 that confers a capacity to colonize tissue. | (78) |
| Promote tumor progression via induction of proinflammatory mediator such as COX2 and IL1, as well as angiogenic cytokine IL8. | (79) | |
| Some S. gallolyticus strains are able to promote host cell proliferation and adhered to colon cancer cells while others are not. Those virulent strains can promote tumor development in AOM-induced mouse model of CRC. | (80) | |
| Enterotoxigenic Bacteroides fragilis (ETBF) | Using a murine model, ETBF induces persistent subclinical colitis and hyperplasia. | (81) |
| B. fragilis toxin (BFT) upregulates spermine oxidase, a polyamine catabolic enzyme, generating reactive oxygen species and thereby DNA damage. | (82) | |
| EBFT induces colitis and tumorigenesis via IL17 induction, activation of STAT3 and recruitment of polymorphonuclear immature myeloid cells on lamina propria. | (83, 84) | |
| pks+ Escherichia coli | colibactin is able to induce DNA double strand breaks and chromosomal instability in human cells. | (85, 86) |
| Fusobacterium nucleatum | F. nucleatum invasion promotes a proinflammatory response in cell lines derived from colon cancer. | (87, 88) |
| FadA allows bacteria attachment and invasion of E-cadherin-expressing cells, induction of human CRC and proinflammatory response associated with NF-kB2 upregulation. | (89) | |
| F. nucleatum avoiding NK-mediated tumor cell lysis via FAP2 interaction with the inhibitory NK-receptor TIGIT. | (90, 91) | |
| Peptostreptococcus anaerobius | Promotes colorectal carcinogenesis through cholesterol synthesis induced by TLR2/TLR4 signaling activation and reactive oxygen species (ROS) generation. | (92) |
| P. anaerobius adheres to the CRC cells and accelerates CRC development in APCMin/+ mice. | (93) | |
| Enterococcus faecalis | Produce hydroxyl radical and extracellular superoxide causing DNA breaks promoting chromosomal instability and increased inflammation. | (94, 95) |
| E. faecalis-infected macrophages induce aneuploidy and tetraploidy in colonic epithelial cells through of soluble mediator. | (96) |