Epigallocatechin-3-gallate interferes with EBV-encoding AP-1 signal transduction pathway.
- Author:
Yan ZHAO
1
;
Hai WANG
;
Xiao-rong ZHAO
;
Fei-jun LUO
;
Min TANG
;
Ya CAO
Author Information
- Publication Type:Journal Article
- MeSH: Carcinoma, Squamous Cell; metabolism; pathology; virology; Catechin; analogs & derivatives; pharmacology; Cell Line, Tumor; Cell Survival; drug effects; Herpesvirus 4, Human; Humans; JNK Mitogen-Activated Protein Kinases; metabolism; MAP Kinase Kinase 4; Mitogen-Activated Protein Kinase Kinases; metabolism; Nasopharyngeal Neoplasms; metabolism; pathology; virology; Phosphorylation; drug effects; Protein Transport; drug effects; Proto-Oncogene Proteins c-jun; metabolism; Signal Transduction; drug effects; Transcription Factor AP-1; metabolism; Viral Matrix Proteins; genetics; metabolism; physiology
- From: Chinese Journal of Oncology 2004;26(7):393-397
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo elucidate the interference effect of Epigallocatechin-3-Gallate (EGCG) on targets of Activator Protein-1 (AP-1) signal transduction pathway activated by EB virus encoded latent membrane protein 1 in nasopharyngeal carcinoma (NPC) cell lines.
METHODSSurvival rate of cells was determined by MTT assay. AP-1 and CyclinD1 activation were analyzed by promoter luciferase reporter system. Nuclear translocation of JNK was analyzed by indirect immunofluorescence. Protein expression and phosphorylation were observed by Western blot.
RESULTSEGCG inhibited the survival of CNE1 and CNE-LMP1 cells and the activity of AP-1 caused by LMP1 in CNE-LMP1 cells. EGCG also inhibited the nuclear translocation of JNK and the phosphorylation of c-Jun. It also inhibited cyclinD1 promoter activity and cyclinD1 expression.
CONCLUSIONEGCG inhibits AP-1, JNK, c-Jun and cyclinD1 which are key targets on AP-1 signal transduction pathway. The results may explain the molecular mechanism of action of EGCG against nasopharyngeal carcinoma.
