The Activation of ERK1/2 Via Tyrosine Kinase Pathway Attenuates TRAIL-induced Apoptosis in HeLa cell.
10.11637/kjpa.2004.17.3.187
- Author:
Yoo Hun NOH
1
;
Myoung Woo LEE
;
Dea Sung KIM
;
Do Yeon LEE
;
Sug Won KIM
;
Yong Koo KANG
;
Dong Seup SOHN
;
Soon Cheol PARK
;
Yoon Hee CHUNG
;
Kyung Yong KIM
;
Sung Su KIM
;
Won Bok LEE
Author Information
1. Department of Anatomy, College of Medicine, College of Medicine, Chung-Ang University, Korea. whitefox@cau.ac.kr
- Publication Type:Original Article
- Keywords:
TRAIL;
ERK1/2;
Tyrosine kinase;
Bcl-2 protein;
Apoptosis
- MeSH:
Apoptosis*;
Cell Death;
Down-Regulation;
Genistein;
HeLa Cells*;
Humans;
Necrosis;
Phosphotransferases;
Protein-Tyrosine Kinases*;
Tyrosine*;
Up-Regulation
- From:Korean Journal of Physical Anthropology
2004;17(3):187-196
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) serves as an extracellular signal triggering apoptosis in tumor cells. To characterize the molecular events involved in TRAIL-induced apoptotic signaling, we investigated the role of extracellular signal-regulated kinase 1/2(ERK1/2) in the apoptosis using HeLa cells. Here we show that TRAIL pronounced ERK1/2 activation through a tyrosine kinase-dependent mechanism, subsequently elevated anti-apoptotic Bcl-2 protein levels. Pretreatment with Genistein, an inhibitor of tyrosine kinase, significantly attenuated ERK1/2 activation and enhanced cell death. Moreover, inhibition of ERK1/2 with PD98059 promoted apoptotic cell death through the down-regulation of ERK1/2 activity and Bcl-2 protein levels. Taken together, our results suggest that the activation of ERK1/2 via tyrosine kinase pathway plays a protective role as the mechanism of cellular defense through the up-regulation of Bcl-2 protein levels in TRAIL-induced apoptosis.
