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Details

Autor(en) / Beteiligte
Titel
LPS promotes the expression of PD‐L1 in gastric cancer cells through NF‐κB activation
Ist Teil von
  • Journal of cellular biochemistry, 2018-12, Vol.119 (12), p.9997-10004
Ort / Verlag
United States: Wiley Subscription Services, Inc
Erscheinungsjahr
2018
Link zum Volltext
Quelle
MEDLINE
Beschreibungen/Notizen
  • Gastric cancers are a group of highly aggressive malignancies with a huge disease burden worldwide. Gastric infections, such as helicobacter pylori, can induce the occurrence of gastric cancers. However, the role of gastric infection in gastric cancer development is unclear. Programmed death‐ligand 1 (PD‐L1, B7‐H1) is a member of the B7 family of cell surface ligands, which binds the PD‐1 transmembrane receptor and inhibits T‐cell activation within cancer tissues. It has been reported that the expression of PD‐L1 is inversely related to the prognosis of patients with gastric cancers. Therefore, the regulation of PD‐L1 expression in gastric cancers needs to be studied. In the current study, we explored the possible effects of lipopolysaccharide (LPS) on PD‐L1 expression in gastric cancer cells. We observed that LPS stimulation could markedly increase PD‐L1 expression in gastric cancer cells. Furthermore, we found that nuclear factor‐κB (NF‐κB) activation was involved in PD‐L1 expression in gastric cancer cells exposed to LPS stimulation through p65‐binding to the PD‐L1 promoter. Taken together, these data indicate that gastric infection might promote the development of gastric cancers thought the LPS‐NF‐κB‐PD‐L1 axis. We observed that lipopolysaccharide (LPS) stimulation could markedly increase programmed death‐ligand 1 (PD‐L1) expression in gastric cancer cells. Furthermore, we found that nuclear factor‐κB (NF‐κB) activation was involved in PD‐L1 expression in gastric cancer cells exposed to LPS stimulation through p65‐binding to the PD‐L1 promoter. Taken together, these data indicate that gastric infection might promote the development of gastric cancers thought the LPS‐NF‐κB‐PD‐L1 axis.

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