LncRNA H19 promotes epithelial mesenchymal transition and metastasis of esophageal cancer via STAT3/EZH2 axis.
Int J Biochem Cell Biol
; 113: 27-36, 2019 08.
Article
em En
| MEDLINE
| ID: mdl-31102664
ABSTRACT
BACKGROUND:
Long non-coding RNA H19 (lncRNA H19) has been widely reported in esophageal cancer (EC), and previous study had found that lncRNAH19 was up-regulated in EC and promoted cell proliferation and metastasis. However, the mechanism still needs further studied.METHODS:
Levels of lncRNA H19 were analyzed by qRT-PCR in matched samples from 30 patients. Expression levels of lncRNA H19, let-7, STAT3 and EZH2 were additionally identified by qRT-PCR and western blotting in five EC cell lines. The effects of lncRNA H19 on cell proliferation, migration, invasion and apoptosis in cell lines were performed by MTT assay, colony formation assay, Transwell assay and flow cytometry in vitro, and tumor formation was detected by xenograft nude mice model in vivo. The expression level of STAT3, EZH2, ß-catenin, and EMT and metastasis related molecules such as E-cadherin, N-cadherin, Snail-1 and MMP-9 was assessed by qRT-PCR and western blotting. Finally, luciferase reporter assay and RIP assay were used to verify the interaction between lncRNA H19 and let-7c, and their subsequent regulation of STAT3.RESULTS:
Knockdown of lncRNA H19 repressed cell proliferation, migration and invasion as well as EMT and metastasis via STAT3-EZH2-ß-catenin pathway, while lncRNA H19 regulated STAT3 negatively regulated let-7c in EC cell lines.CONCLUSIONS:
lncRNA H19 facilitates EMT and metastasis of EC through let-7c/STAT3/EZH2/ß-catenin axis.Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Neoplasias Esofágicas
/
Fator de Transcrição STAT3
/
RNA Longo não Codificante
/
Proteína Potenciadora do Homólogo 2 de Zeste
Tipo de estudo:
Prognostic_studies
Limite:
Animals
/
Female
/
Humans
/
Male
Idioma:
En
Revista:
Int J Biochem Cell Biol
Assunto da revista:
BIOQUIMICA
Ano de publicação:
2019
Tipo de documento:
Article