Article Figures & Data
Figures
- Figure 1
- Imbalance of gut microbiota via diet, infections, nutrition, and xenobiotic.
- Figure 2
- Effects of gut microbiota on nutrition.
Tables
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 immunityPeptostreptococcus anaerobius - Induces TLR2/4 that causes ROS activation
- Promotes cholesterol synthesis
- Induces cell proliferationPeptostreptococcus stomatis - Induces hypoxia
- Produces CMS-1Prevotella 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 proliferationStreptococcus 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
Bacterial metabolites Examples Effect on CRC SCFAs Butyrate, propionate, and acetate - Immunomodulation via regulation of AhR
- Rebalance gut microbiota diversity and composition
- Inhibit NF-kB and activate apoptosis
- Antitumor effect via modulation of Tc17 cells and CTLs
- Inhibit ERK1/2, causing tumor growth disruption
- Induce ROS activity and decrease glucose oxidation
- Induce HDACBile acid Primary and secondary bile acids - Bind to FXR as CRC inhibitor
- Promote cancer initiation by upregulating IL-8, ERK1/2, and inhibiting STAT3 phosphorylation
- Activate MAPK pathway via upregulation of uPAR and calcium signalingLactate - Creates an acidification environment
- Stimulates angiogenic response to oxygen transfer, glucose delivery and nutrition delivery that promote CRC invasion, proliferation, and migrationSuccinate - Inhibits CRC proliferation and induces CRC metastasis via SUCNR1 signaling Protein-derived metabolites HO-PAA, PAA, phenol (produced from tyrosine), acetaldehyde, H2S, and NOCs - Hydrogen sulfide inhibits the anti-inflammatory outcome in CRC cell lines by activating NF-kB pathway signaling
- NOCs contribute to K-ras mutation, which drives CRC proliferationSCFAs: short-chain fatty acids, HO-PAA: 4-hydroxyphenylacetic acid, PAA: phenylacetic acid, H2S: hydrogen sulfide, NOCs: N-nitroso compounds, AhR: aryl hydrocarbon receptor, NF-kB: nuclear factor kappa B, Tc17: IL-17-secreting CD8 T cells), CTLs: cytotoxic T lymphocytes, ERK1/2: protein kinases 1 and 2, ROS: reactive oxygen species, HDAC: histone deacetylases, FXR: farnesoid X receptor, CRC: colorectal cancer, IL: interleukin, STAT3: Signal Transducer and Activator of Transcription 3, MAPK: mitogen-activated protein kinase, uPAR: urokinase plasminogen activator, SUCNR1: succinate receptor 1, K-ras: Kirsten rat sarcoma viral oncogene homolog
In this issue
Jump to section
Related Articles
Cited By...
- No citing articles found.