Bacteria-Cancer Interface: Awaiting the Perfect Storm.
Jonathan Pommer HansenWaled Mohammed AliRajeeve SivadasanKarthika RajeevePublished in: Pathogens (Basel, Switzerland) (2021)
Epidemiological evidence reveal a very close association of malignancies with chronic inflammation as a result of persistent bacterial infection. Recently, more studies have provided experimental evidence for an etiological role of bacterial factors disposing infected tissue towards carcinoma. When healthy cells accumulate genomic insults resulting in DNA damage, they may sustain proliferative signalling, resist apoptotic signals, evade growth suppressors, enable replicative immortality, and induce angiogenesis, thus boosting active invasion and metastasis. Moreover, these cells must be able to deregulate cellular energetics and have the ability to evade immune destruction. How bacterial infection leads to mutations and enriches a tumour-promoting inflammatory response or micro-environment is still not clear. In this review we showcase well-studied bacteria and their virulence factors that are tightly associated with carcinoma and the various mechanisms and pathways that could have carcinogenic properties.
Keyphrases
- induced apoptosis
- dna damage
- inflammatory response
- oxidative stress
- cell cycle arrest
- cell death
- escherichia coli
- staphylococcus aureus
- pseudomonas aeruginosa
- genome wide
- endoplasmic reticulum stress
- immune response
- dna repair
- signaling pathway
- vascular endothelial growth factor
- gene expression
- cell proliferation
- dna methylation
- toll like receptor
- copy number
- wound healing
- solid state