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Toxins (Basel)
2017[Mar]; 9
(4
): ? PMID28350359
show ga
Gastric cancer is a leading cause of cancer death worldwide. Diet, obesity,
smoking and chronic infections, especially with Helicobacter pylori, contribute
to stomach cancer development. H. pylori possesses a variety of virulence factors
including encoded factors from the cytotoxin-associated gene pathogenicity island
(cagPAI) or vacuolating cytotoxin A (VacA). Most of the cagPAI-encoded products
form a type 4 secretion system (T4SS), a pilus-like macromolecular transporter,
which translocates CagA into the cytoplasm of the host cell. Only H. pylori
strains carrying the cagPAI induce the transcription factor NF-?B, but CagA and
VacA are dispensable for direct NF-?B activation. NF-?B-driven gene products
include cytokines/chemokines, growth factors, anti-apoptotic factors,
angiogenesis regulators and metalloproteinases. Many of the genes transcribed by
NF-?B promote gastric carcinogenesis. Since it has been shown that
chemotherapy-caused cellular stress could elicit activation of the survival
factor NF-?B, which leads to acquisition of chemoresistance, the NF-?B system is
recommended for therapeutic targeting. Research is motivated for further search
of predisposing conditions, diagnostic markers and efficient drugs to improve
significantly the overall survival of patients. In this review, we provide an
overview about mechanisms and consequences of NF-?B activation in gastric mucosa
in order to understand the role of NF-?B in gastric carcinogenesis.
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