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Toxins 2017, 9(4), 119; doi:10.3390/toxins9040119

NF‐κB Signaling in Gastric Cancer

Institute of Experimental Internal Medicine, Otto von Guericke University Magdeburg, Magdeburg 39120, Germany
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Received: 3 February 2017 / Revised: 14 March 2017 / Accepted: 22 March 2017 / Published: 28 March 2017
(This article belongs to the Special Issue H. pylori Virulence Factors in the Induction of Gastric Cancer)
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Abstract

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‐κB, but CagA and VacA are dispensable for direct NF‐κB activation. NF‐κB‐driven gene products include cytokines/chemokines, growth factors, anti‐apoptotic factors, angiogenesis regulators and metalloproteinases. Many of the genes transcribed by NF‐κB promote gastric carcinogenesis. Since it has been shown that chemotherapy‐caused cellular stress could elicit activation of the survival factor NF‐κB, which leads to acquisition of chemoresistance, the NF‐κB 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‐κB activation in gastric mucosa in order to understand the role of NF‐κB in gastric carcinogenesis. View Full-Text
Keywords: NF‐κB; inflammation; gastric cancer; Helicobacter pylori; VacA toxin; Type 4 secretion system; tumor microenvironment; chemoresistance NF‐κB; inflammation; gastric cancer; Helicobacter pylori; VacA toxin; Type 4 secretion system; tumor microenvironment; chemoresistance
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Sokolova, O.; Naumann, M. NF‐κB Signaling in Gastric Cancer. Toxins 2017, 9, 119.

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