- Bacteria associated with colorectal cancer.
| Bacteria | Association with colorectal cancer |
|---|---|
| Fusobacterium nucleatum | - Stages, recurrence, and patients’ low survival rates - Prevalence of a molecular feature such as mutation of BRAF, hypermutation with microsatellite instability and metastases - Serrated pathway manipulation - Binds to the E-cadherins’s extracellular domain and induces cancer cell proliferation - Promotes autophagy by upregulating CARD3 - Regulates microRNA to induce chemotherapy resistance - Inhibits T-cell infiltration and stimulates myeloid-derived immunity |
| Peptostreptococcus anaerobius | - Induces TLR2/4 that causes ROS activation - Promotes cholesterol synthesis - Induces cell proliferation |
| Peptostreptococcus stomatis | - Induces hypoxia - Produces CMS-1 |
| Prevotella intermedia | Mutates P53 in pancreatic cancer |
| Parvimonas micra | Interrupts NOD2 that is involved in chemotherapy resistance and cancer progression |
| Bacteroides fragilis | - Regulates STAT3 and NF-kB that modulate pro-inflammatory molecules such as cytokine IL-17 - Interrupts E-cadherin and DNA damage - Induces COX-2, causing upregulation of PGE2 and promotion of inflammation and cell proliferation |
| Streptococcus gallolyticus | Induces pro-inflammatory markers such as NF-κB and IL-8 |
| Escherichia coli | Induces chromosomal appearance |
BRAF: B-Raf Proto-Oncogene, Serine/Threonine Kinase, CARD3: caspase activation and recruitment domain 3, TLR: toll-like receptor, ROS: reactive oxygen species, CMS-1: consensus molecular subtype-1, P53: tumor protein p53, NOD2: nucleotide-binding oligomerization domain 2, STAT3: Signal Transducer And Activator Of Transcription 3, NF-kB: nuclear factor kappa B, IL: interleukin, COX-2: cyclooxygenase-2, PGE2: prostaglandin E2