Claudin-6 is down-regulated in gastric cancer and its potential pathway.
BGC-823
Gastric cancer
JNK pathway
claudin-6
differentiation
Journal
Cancer biomarkers : section A of Disease markers
ISSN: 1875-8592
Titre abrégé: Cancer Biomark
Pays: Netherlands
ID NLM: 101256509
Informations de publication
Date de publication:
2020
2020
Historique:
pubmed:
12
5
2020
medline:
30
1
2021
entrez:
12
5
2020
Statut:
ppublish
Résumé
Claudins are indispensible in modulating the permeability of epithelial and endothelial cells and in the maintenance of cell polarity. In order to verify the function of claudin-6 in the development of gastric cancer, we investigated claudin-6 expression in different gastric disease tissues. Moreover, we further explored whether overexpression of claudin-6 altered proliferation, apoptosis, migration, invasiveness, differentiation in BGC-823 cells and the potential mechanism. Immunohistochemistry was performed to detect the in situ expression of claudin-6 in different gastric disease tissues; moreover, cell culture, real-time PCR and western blot were used to evaluate the effect of overexpression of claudin-6 in vitro and the related mechanism. The results of immunohistochemical staining showed that the positivity of claudin-6 was significantly higher in superficial gastritis than that in gastric cancer. Overexpression of claudin-6 induced differentiation of BGC-823 cells by inhibiting the JNK pathway. However, it had no effect on proliferation, apoptosis, migration or invasiveness in vitro. The expression of claudin-6 was decreased in gastric cancer. Overexpression of claudin-6 induced differentiation of gastric cancer cells by inhibiting the JNK pathway.
Identifiants
pubmed: 32390606
pii: CBM201554
doi: 10.3233/CBM-201554
doi:
Substances chimiques
Claudins
0
claudin 6
MRC5FX426I
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM