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Upregulation of Beclin-1 expression and phosphorylation of Bcl-2 and p53 are involved in the JNK-mediated autophagic cell death.

Authors
Park, KJ; Lee, SH; Lee, CH; Jang, JY; Chung, J; Kwon, MH; Kim, YS
Citation
Biochemical and biophysical research communications, 382(4):726-729, 2009
Journal Title
Biochemical and biophysical research communications
ISSN
0006-291X1090-2104
Abstract
Though the activation of c-Jun NH2-terminal kinase (JNK) has been reported to be essential for autophagic cell death in response to various stressors, the molecular links between JNK activation and autophagic cell death signaling remain elusive. Here we report that, in the JNK-dependent autophagic cell death of HCT116 cells induced by an agonistic single chain variable fragment antibody, HW1, against human death receptor 5 (DR5), JNK activation upregulated Beclin-1 expression and induced Bcl-2 and p53 phosphorylation. Further, the p53-deficient HCT116 cells showed less susceptibility to the HW1-mediated autophagic cell death than the wild type cells, suggesting that JNK-mediated p53 phosphorylation promotes the autophagic cell death. Our results suggest that DR5-stimulated JNK activation and its consequent fluxes into the pro-autophagic signaling pathways contribute to the autophagic cell death in cancer cells.
MeSH terms
Apoptosis Regulatory Proteins/biosynthesis*Autophagy*Cell Line, TumorHumansJNK Mitogen-Activated Protein Kinases/metabolismMembrane Proteins/biosynthesis*PhosphorylationProto-Oncogene Proteins c-bcl-2/metabolism*Receptors, TNF-Related Apoptosis-Inducing Ligand/agonistsTumor Suppressor Protein p53/metabolism*Up-Regulation
DOI
10.1016/j.bbrc.2009.03.095
PMID
19318089
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Microbiology
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