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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

Cited 82 time in Web of Science Cited 85 time in Scopus
Authors
Park, Kyung-Jin; Lee, Seung-Hyun; Lee, Chang-Han; Jang, Ji-Young; Kwon, Myung-Hee; Kim, Yong-Sung; Chung, Junho
Issue Date
2009-05-15
Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
Citation
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS; Vol.382(4); 726-729
Keywords
Autophagic cell deathBeclin-1 upregulationJNK activationBcl-2 phosphorylationp53 phosphorylation
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.
ISSN
0006-291X
Language
English
URI
http://hdl.handle.net/10371/77731
DOI
https://doi.org/10.1016/j.bbrc.2009.03.095
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College of Medicine/School of Medicine (의과대학/대학원)Dept. of Biochemistry & Molecular Biology (생화학교실)Journal Papers (저널논문_생화학교실)
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