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JNK Promotes Epithelial Cell Anoikis by Transcriptional and Post-translational Regulation of BH3-Only Proteins.

Cell reports | Nov 14, 2017

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.

Pubmed ID: 29141222 RIS Download

Mesh terms: Animals | Anoikis | Apoptosis Regulatory Proteins | Cell Line | Epithelial Cells | Female | Humans | JNK Mitogen-Activated Protein Kinases | Male | Mice | Mice, Inbred C57BL | Protein Processing, Post-Translational

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Associated grants

  • Agency: NIDDK NIH HHS, Id: R01 DK107220
  • Agency: NIDDK NIH HHS, Id: R01 DK112698

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