Identification of ADP-ribosylation factor 4 as a suppressor of N-(4-hydroxyphenyl)retinamide-induced cell death
- Authors
- Woo, Im Sun; Eun, So Young; Jang, Han-Su; Kang, Eun Sil; Kim, Gil Hyeong; Kim, Hye Jung; Lee, Jae Heun; Chang, Ki Churl; Kim, Jin-Hoi; Han, Chang Woo; Seo, Han Geuk
- Issue Date
- 8-Apr-2009
- Publisher
- ELSEVIER IRELAND LTD
- Keywords
- 4-HPR; ARF4; Reactive oxygen species; Apoptosis; Bax; JNK
- Citation
- CANCER LETTERS, v.276, no.1, pp.53 - 60
- Indexed
- SCIE
SCOPUS
- Journal Title
- CANCER LETTERS
- Volume
- 276
- Number
- 1
- Start Page
- 53
- End Page
- 60
- URI
- https://scholarworks.bwise.kr/gnu/handle/sw.gnu/26323
- DOI
- 10.1016/j.canlet.2008.10.031
- ISSN
- 0304-3835
- Abstract
- Yeast-based functional screening for inhibitors of Bcl-2-associated X protein (Bax)-induced cell death in yeast identified ADP-ribosylation factor 4 (ARF4) as a novel anti-apoptotic gene in human glioblastoma-derived U373MG cells. Yeast or U373MG cells that overexpressed ARF4 exhibited reduced reactive oxygen species (ROS) generation in response to Bax or N-(4-hydroxyphenyl)retinamide (4-HPR), respectively, which suggests that ROS play a role in the inhibition of cell death by ARF4. The 4-HPR-mediated phosphorylation of c-JUN N-terminal kinase, p38, and extracellular signal-regulated kinase was markedly suppressed in U373MG cells that stably expressed ARF4. Stable ARF4 transfectants were also refractory to 4-HPR-induced mitochondrial translocation of Bax, release of mitochondrial cytochrome c, and activation of caspase-3. Our results suggest that ARF4 participates in the regulation of glioblastoma apoptosis through the inhibition of stress-mediated apoptotic signals. (C) 2008 Elsevier Ireland Ltd. All rights reserved.
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