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Non-canonical β-catenin degradation mediates reactive oxygen species-induced epidermal cell death
被引:10
作者:
Omori, E.
[1
]
Matsumoto, K.
[2
]
Ninomiya-Tsuji, J.
[1
]
机构:
[1] N Carolina State Univ, Dept Environm & Mol Toxicol, Raleigh, NC 27695 USA
[2] Nagoya Univ, Grad Sch Sci, Dept Mol Biol, Nagoya, Aichi 4648601, Japan
来源:
基金:
美国国家卫生研究院;
关键词:
apoptosis;
beta-catenin;
caspase;
epidermis;
reactive oxygen species;
TUMOR-NECROSIS-FACTOR;
IL-1 SIGNALING PATHWAY;
PROTEOLYTIC CLEAVAGE;
FACTOR-ALPHA;
KINASE TAK1;
HELA-CELLS;
TNF-ALPHA;
KAPPA-B;
ACTIVATION;
APOPTOSIS;
D O I:
10.1038/onc.2011.49
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
beta-Catenin is constantly degraded through the ubiquitin-proteasomal pathway. In this study, we report that a different type of beta-catenin degradation is causally involved in epidermal cell death. We observed that reactive oxygen species (ROS) caused beta-catenin degradation in the epidermal cells through a caspase-dependent mechanism, which results in disruption of cell adhesion. Disruption of cell adhesion increased ROS and activated caspases. Upregulation of the intact beta-catenin blocked ROS accumulation and caspase activation. These results indicate that a feed-forward loop consisting of ROS, caspases activation and beta-catenin degradation induces epidermal cell death. Oncogene (2011) 30, 3336-3344; doi:10.1038/onc.2011.49; published online 7 March 2011
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页码:3336 / 3344
页数:9
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