Gastric cancer: genome damaged by bugs.
Yanan ZhaoJinglin ZhangAlfred S L ChengJun YuKa Fai ToWei KangPublished in: Oncogene (2020)
Gastric cancer (GC) is one of the leading causes of cancer-related death worldwide. The role of the microorganisms in gastric tumorigenesis attracts much attention in recent years. These microorganisms include bacteria, virus, and fungi. Among them, Helicobacter pylori (H. pylori) infection is by far the most important risk factor for GC development, with special reference to the early-onset cases. H. pylori targets multiple cellular components by utilizing various virulence factors to modulate the host proliferation, apoptosis, migration, and inflammatory response. Epstein-Barr virus (EBV) serves as another major risk factor in gastric carcinogenesis. The virus protein, EBER noncoding RNA, and EBV miRNAs contribute to the tumorigenesis by modulating host genome methylation and gene expression. In this review, we summarized the related reports about the colonized microorganism in the stomach and discussed their specific roles in gastric tumorigenesis. Meanwhile, we highlighted the therapeutic significance of eradicating the microorganisms in GC treatment.
Keyphrases
- epstein barr virus
- helicobacter pylori
- early onset
- diffuse large b cell lymphoma
- gene expression
- inflammatory response
- late onset
- genome wide
- dna methylation
- signaling pathway
- helicobacter pylori infection
- gas chromatography
- escherichia coli
- risk factors
- oxidative stress
- lipopolysaccharide induced
- pseudomonas aeruginosa
- cell death
- cell cycle arrest
- mass spectrometry
- working memory
- antimicrobial resistance
- immune response
- high resolution
- protein protein
- toll like receptor
- emergency department
- combination therapy
- binding protein
- pi k akt
- electronic health record
- disease virus