| Liu JD |
------>authors3_c=None ------>paper_class1=1 ------>Impact_Factor=None ------>paper_class3=2 ------>paper_class2=1 ------>vol=37 ------>confirm_bywho=ncchang ------>insert_bywho=jdliu ------>Jurnal_Rank=None ------>authors4_c=None ------>comm_author= ------>patent_EDate=None ------>authors5_c=None ------>publish_day=None ------>paper_class2Letter=None ------>page2=24 ------>medlineContent= ------>unit=E0109 ------>insert_date=20040504 ------>iam=1 ------>update_date=None ------>author=??? ------>change_event=5 ------>ISSN=None ------>authors_c=None ------>score=462 ------>journal_name=Molecular Carcinogenesis ------>paper_name=Involvement of c-Jun N-Terminal Kinase Activation in 15-Deoxy-? 12,14-Prostaglandin J2 and Prostaglandin A1-Induced Apoptosis in AGS Gastric Epithelial Cells ------>confirm_date=20040504 ------>tch_id=064006 ------>pmid=12720296 ------>page1=16 ------>fullAbstract=Cyclopentenone prostaglandins (CyPGs), derivatives of arachidonic acid, have been suggested to exert growth-inhibitory activity through peroxisome proliferator-activated receptor (PPAR)-dependent and -independent mechanisms. Here we examined various eicosanoids for growth inhibition and found that the terminal derivative of prostaglandin (PG) J(2) metabolism, 15-deoxy-Delta(12,14)-PGJ(2) (15d-PGJ(2)), and PGA(1) markedly inhibited the growth and induced apoptosis in AGS gastric carcinoma cells. There were no significant increases in cell death and DNA-fragmentation in the cells with overexpression of PPARalpha or PPARgamma, indicating the possibility that 15d-PGJ(2) and PGA(1) induced apoptosis through PPAR-independent pathway. Moreover, 15d-PGJ(2) and PGA(1) activated the c-jun N-terminal kinase (JNK) and caspase-3 activity in dose- and time-dependent manners. To examine further the role of JNK signaling cascades in apoptosis induced by 15d-PGJ(2) and PGA(1), we transfected dominant-negative (DN) mutants of JNK plasmid into the cells to analyze the apoptotic characteristics of cells overexpressing DN-JNK following exposure to 15d-PGJ(2) and PGA(1). Overexpression of DN-JNK significantly repressed both endogenous JNK and caspase-3 activity, and subsequently decreased apoptosis induced by 15d-PGJ(2) and PGA(1). These results suggested that CyPGs, such as 15d-PGJ(2) and PGA(1), activated JNK signaling pathway, and that JNK activation may be involved in 15d-PGJ(2)- and PGA(1)-induced apoptosis. ------>tmu_sno=None ------>sno=8968 ------>authors2=Lin SY ------>authors3=Mo YS ------>authors4=Hung LF ------>authors5=Tsai SH ------>authors6=Lin JK, Liang YC ------>authors6_c=None ------>authors=Liu JD ------>delete_flag=0 ------>SCI_JNo=None ------>authors2_c=None ------>publish_area=None ------>updateTitle=Involvement of c-jun N-terminal kinase activation in 15-deoxy-delta12,14-prostaglandin J2-and prostaglandin A1-induced apoptosis in AGS gastric epithelial cells. ------>language=2 ------>check_flag=None ------>submit_date=None ------>country=None ------>no= ------>patent_SDate=None ------>update_bywho=None ------>publish_year=2003 ------>submit_flag=None ------>publish_month=None |