IL-37 suppresses migration and invasion of gallbladder cancer cells through inhibition of HIF-1α induced epithelial-mesenchymal transition.
Eur Rev Med Pharmacol Sci
; 22(23): 8179-8185, 2018 12.
Article
de En
| MEDLINE
| ID: mdl-30556856
ABSTRACT
OBJECTIVE:
Gallbladder carcinoma (GBC) is the seventh most common cancer across the globe and the most common malignancy of the biliary tract. Epithelial-mesenchymal transition (EMT) is an important pre-requisite for tumor metastasis; however, its mechanism in GBC has not yet been defined. In the present study, we investigated the effects of interleukin-37 (IL-37) on the epithelial-mesenchymal transition (EMT) of gallbladder cancer cells. MATERIALS ANDMETHODS:
RT-qPCR and Western blotting were used to determine the expression of IL-37 in GBC cancer cells and non-tumorigenic human intra-hepatic biliary epithelial cell line. Western blotting was also used for detecting the expression of vimentin, Snail, and E-cadherin.RESULTS:
Expression level of IL-37 in GBC cells was decreased in GBC cancer cells compared with the non-tumorigenic human intra-hepatic biliary epithelial cell line. Decreased expression of vimentin and Snail and increased expression of E-cadherin were found in the groups which overexpress IL-37 when compared with the control. Mechanism study showed that IL-37 suppressed the expression of HIF1α in cells. However, HIF1α stabilization by CoCl2 could attenuate the function of IL-37.CONCLUSIONS:
Our results indicate that IL-37 plays an antitumor role during the progression of gallbladder carcinoma. IL-37 could inhibit HIF1α induced EMT. Our data provide a new strategy for the treatment of gallbladder cancer.
Texte intégral:
1
Collection:
01-internacional
Base de données:
MEDLINE
Sujet principal:
Mouvement cellulaire
/
Interleukine-1
/
Sous-unité alpha du facteur-1 induit par l'hypoxie
/
Transition épithélio-mésenchymateuse
/
Tumeurs de la vésicule biliaire
Limites:
Humans
Langue:
En
Journal:
Eur Rev Med Pharmacol Sci
Sujet du journal:
FARMACOLOGIA
/
TOXICOLOGIA
Année:
2018
Type de document:
Article