PLCE1 Promotes the Invasion and Migration of Esophageal Cancer Cells by Up-Regulating the PKCα/NF-κB Pathway
Yonsei Medical Journal
;
: 1159-1165, 2018.
Artigo
em Inglês
| WPRIM
| ID: wpr-718496
ABSTRACT
PURPOSE:
To investigate the effect and mechanism of phospholipase C epsilon gene 1 (PLCE1) expression on esophageal cancer cell lines. MATERIALS ANDMETHODS:
The esophageal carcinoma cell lines Eca109 and EC9706 and normal esophageal epithelial cell line HEEC were cultured. The expression of PLCE1, protein kinase C alpha (PKCα), and nuclear factor kappa B (NF-κB) p50/p65 homodimer in cells were comparatively analyzed. The esophageal cancer cells were divided into si-PLCE1, control siRNA (scramble), and mock groups that were transfected with specific siRNA for PLCE1, control siRNA, and blank controls, respectively. Expression of PLCE1, PKCα, p50, and p65 was detected by Western blotting. Transwell assay was used to detect migration and invasion of Eca109 and EC9706 cells.RESULTS:
Compared with HEEC, the expression of PLCE1, PKCα, p50, and p65 was increased in Eca109 and EC9706 cells. The expression of PLCE1 was positively correlated with the expression of PKCα and p50 (PKCα r=0.6328, p=0.032; p50 r=0.6754, p=0.041). PKCα expression had a positive correlation with the expression of p50 and p65 (p50 r=0.9127, p=0.000; p65 r=0.9256, p=0.000). Down-regulation of PLCE1 significantly decreased the expression of PKCα and NF-κB-related proteins (p65 p=0.002, p=0.004; p50 p=0.005, p=0.009) and inhibited the migration and invasion of Eca109 and EC9706 cells.CONCLUSION:
PLCE1 activated NF-κB signaling by up-regulating PKCα, which could promote invasion and migration of esophageal cancer cells.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Fosfolipases Tipo C
/
Neoplasias Esofágicas
/
Regulação para Baixo
/
Linhagem Celular
/
Western Blotting
/
NF-kappa B
/
RNA Interferente Pequeno
/
Células Epiteliais
/
Proteína Quinase C-alfa
Idioma:
Inglês
Revista:
Yonsei Medical Journal
Ano de publicação:
2018
Tipo de documento:
Artigo
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