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Sodium orthovanadate potentiates EGCG-induced apoptosis that is dependent on the ERK pathway

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Author(s)
Yun-Jung ChoiSung-Yup LimJu-Hyung WooYoung-Ho KimYoung Kyu KwonSeong-Il SuhSung-Hee LeeWha-Youl ChoiJong-Guk KimIn-Seon LeeJong-Wook ParkTaeg Kyu Kwon
Keimyung Author(s)
Park, Jong WookKwon, Taeg KyuSuh, Seong Il
Department
Dept. of Immunology (면역학)
Dept. of Microbiology (미생물학)
Journal Title
Biochemical and Biophysical Research Communications
Issued Date
2003
Volume
305
Issue
1
Abstract
Epigallocatechin-3-gallate (EGCG) is a potent chemopreventive agent in many test systems and has been shown to inhibit tumor promotion and induce apoptosis. In the present study, we determined the effect of vanadate, a potent inhibitor of tyrosine phosphatase, on EGCG-induced apoptosis. Investigation of the mechanism of EGCG or vanadate-induced apoptosis revealed induction of caspase 3 activity and cleavage of phospholipase-γ1 (PLC-γ1). Furthermore, vanadate potentiated EGCG-induced apoptosis by mitogen-activated protein kinase (MAPK) signaling pathway. Treatment with EGCG plus vanadate for 24 h produced morphological features of apoptosis and DNA fragmentation in U937 cells. This was associated with cytochrome c release, caspase 3 activation, and PLC-γ1 degradation. EGCG plus vanadate activates multiple signal transduction pathways involved in coordinating cellular responses to stress. We demonstrate a requirement for extracellular signal-regulated protein kinase (ERK), a member of the mitogen-activated protein kinase family in EGCG plus vanadate-induced apoptosis in U937 cells. Elevated ERK activity that contributed to apoptosis by EGCG plus vanadate was supported by PD98059 and U0126, chemical inhibitor of MEK/ERK signaling pathway, prevented apoptosis. Taken together, our finding suggests that ERK activation plays an active role in mediating EGCG plus vanadate-induced apoptosis of U937 cells and functions upstream of caspase activation to initiate the apoptotic signal.

Keywords
EGCG;
Vanadate;
U937 cells;
Apoptosis;
Caspase 3;
ERK
Keimyung Author(s)(Kor)
박종욱
권택규
서성일
Publisher
School of Medicine
Citation
Yun-Jung Choi et al. (2003). Sodium orthovanadate potentiates EGCG-induced apoptosis
that is dependent on the ERK pathway. Biochemical and Biophysical Research Communications, 305(1), 176–185. doi: 10.1016/S0006-291X(03)00719-8
Type
Article
ISSN
0006-291X
Source
https://linkinghub.elsevier.com/retrieve/pii/S0006291X03007198
DOI
10.1016/S0006-291X(03)00719-8
URI
https://kumel.medlib.dsmc.or.kr/handle/2015.oak/35172
Appears in Collections:
1. School of Medicine (의과대학) > Dept. of Immunology (면역학)
1. School of Medicine (의과대학) > Dept. of Microbiology (미생물학)
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