[Phosphorylated JNK mediated apoptosis induced by all trans retinoid acid in human retinoblastoma cell line].
OBJECTIVE
To investigate the mechanism of all trans retinoid acid (ATRA) inhibition of cell growth and induction of apoptosis in human retinoblastoma Y79 cells.


METHODS
Antiproliferating 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.


RESULTS
After 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.


CONCLUSIONS
ATRA can induce the apoptosis in Y79 cells by phosphorylation of JNK, which suggests that ATRA may have clinical application prospects for treatment of retinoblastoma.
Min
Hong-bo
HB
Department of Ophthalmology, 455 Hospital, PLA, Shanghai 200052, China.
Wang
Jian-wen
JW
Sun
Ji-hu
JH
Bu
Shi-zhong
SZ
Huang
Qin
Q
D000970:Antineoplastic Agents / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects*; D002453:Cell Cycle / Q000187:drug effects; D045744:Cell Line, Tumor; D005434:Flow Cytometry; D006801:Humans; D048031:JNK Mitogen-Activated Protein Kinases / Q000502:physiology*; D010766:Phosphorylation; D012175:Retinoblastoma / Q000188:drug therapy* / Q000473:pathology; D013936:Thymidine / Q000378:metabolism; D014212:Tretinoin / Q000494:pharmacology*
D000970:Antineoplastic Agents; D014212:Tretinoin; D048031:JNK Mitogen-Activated Protein Kinases; D013936:Thymidine