Phosphorylated JNK mediated apoptosis induced by all trans retinoid acid in human retinoblastoma cell line.
- Author:
Hong-bo MIN
1
;
Jian-wen WANG
;
Ji-hu SUN
;
Shi-zhong BU
;
Qin HUANG
Author Information
- Publication Type:Journal Article
- MeSH: Antineoplastic Agents; pharmacology; Apoptosis; drug effects; Cell Cycle; drug effects; Cell Line, Tumor; Flow Cytometry; Humans; JNK Mitogen-Activated Protein Kinases; physiology; Phosphorylation; Retinoblastoma; drug therapy; pathology; Thymidine; metabolism; Tretinoin; pharmacology
- From: Chinese Journal of Oncology 2003;25(2):130-133
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the mechanism of all trans retinoid acid (ATRA) inhibition of cell growth and induction of apoptosis in human retinoblastoma Y79 cells.
METHODSAntiproliferating effects of ATRA on Y79 cells were studied by (3)H-thymidine incorporation. Cell cycle analysis was performed by flow cytometry, apoptosis of the ATRA-treated cells was determined by DNA fragmentation analysis and JNK phosphorylation analyzed by Western blot.
RESULTSAfter 36h treatment of 1 micro mol/L ATRA, (3)H-thymidine incorporation decreased to 40% with Y79 cells arrested in G(0)/G(1) and Sub-G(1) peak appeared. DNA ladder was observed in DNA fragmentation analysis after 36h treatment of ATRA. Curcumin, a JNK blocker, blocked the apoptosis and the growth inhibition induced by ATRA. JNK was phosphorylated in 10 to 20 min.
CONCLUSIONATRA can induce the apoptosis in Y79 cells by phosphorylation of JNK, which suggests that ATRA may have clinical application prospects for treatment of retinoblastoma.
