S-Space College of Medicine/School of Medicine (의과대학/대학원) Pharmacology (약리학전공) Journal Papers (저널논문_약리학전공)
The activation of ERK1/2 via a tyrosine kinase pathway attenuates trail-induced apoptosis in HeLa cells
- Lee, Myoung Woo; Bach, Jae Hyun; Lee, Hyun Jung; Lee, Do Yeon; Joo, Wan Seok; Kim, Yong Sik; Park, Soon Cheol; Kim, Kyung Yong; Lee, Won Bok; Kim, Sung Su
- Issue Date
- Taylor & Francis
- Cancer Invest. 2005;23(7):586-92.
- *Apoptosis; Apoptosis Regulatory Proteins/*physiology; Down-Regulation; Enzyme Activation; Genes, bcl-2; Hela Cells; Humans; Membrane Glycoproteins/*physiology; Mitogen-Activated Protein Kinase 3/*metabolism; Protein-Tyrosine Kinases/metabolism; Signal Transduction; TNF-Related Apoptosis-Inducing Ligand; Tumor Necrosis Factor-alpha/*physiology; Up-Regulation
- Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) serves as an extracellular signal that triggers 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 HeLa cell death. Here we show that TRAIL-activated ERK1/2 through a tyrosine kinase-dependent pathway, subsequently elevated anti-apoptotic Bcl-2 protein levels. ERK1/2 inhibition with PD98059 promoted apoptotic cell death through the downregulation of ERK1/2 activity and Bcl-2 protein levels. Moreover, tyrosine kinase inhibition with Genistein in TRAIL-induced apoptosis effectively attenuated ERK1/2 activity and enhanced apoptotic cell death. Taken together, our results indicate that ERK1/2 activation via tyrosine kinase pathway plays a protective role as the cellular defense mechanism through the upregulation of Bcl-2 protein levels in TRAIL-induced apoptosis.
- 0735-7907 (Print)
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