JNK Promotes Epithelial Cell Anoikis by Transcriptional and Post-translational Regulation of BH3-Only Proteins
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Document Type
Journal ArticlePublication Date
2017-11-14Keywords
BAKBAX
BH3-only protein
BIM
BMF
JNK
anoikis
apoptosis
epithelial cell
mammary gland
Biochemistry
Cell Biology
Cellular and Molecular Physiology
Molecular Biology
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Show full item recordAbstract
Developmental morphogenesis, tissue injury, and oncogenic transformation can cause the detachment of epithelial cells. These cells are eliminated by a specialized form of apoptosis (anoikis). While the processes that contribute to this form of cell death have been studied, the underlying mechanisms remain unclear. Here, we tested the role of the cJUN NH2-terminal kinase (JNK) signaling pathway using murine models with compound JNK deficiency in mammary and kidney epithelial cells. These studies demonstrated that JNK is required for efficient anoikis in vitro and in vivo. Moreover, JNK-promoted anoikis required pro-apoptotic members of the BCL2 family of proteins. We show that JNK acts through a BAK/BAX-dependent apoptotic pathway by increasing BIM expression and phosphorylating BMF, leading to death of detached epithelial cells.Source
Cell Rep. 2017 Nov 14;21(7):1910-1921. doi: 10.1016/j.celrep.2017.10.067. Link to article on publisher's siteDOI
10.1016/j.celrep.2017.10.067Permanent Link to this Item
http://hdl.handle.net/20.500.14038/36624PubMed ID
29141222Related Resources
Link to Article in PubMedRights
© 2017 The Author(s).Distribution License
http://creativecommons.org/licenses/by-nc-nd/4.0/ae974a485f413a2113503eed53cd6c53
10.1016/j.celrep.2017.10.067