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Cell Extrusion: A Stress-Responsive Force for Good or Evil in Epithelial Homeostasis

Developmental cell, 2018-02, Vol.44 (3), p.284-296 [Tạp chí có phản biện]

2018 Elsevier Inc. ;Copyright © 2018 Elsevier Inc. All rights reserved. ;ISSN: 1534-5807 ;EISSN: 1878-1551 ;DOI: 10.1016/j.devcel.2018.01.009 ;PMID: 29408235

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  • Nhan đề:
    Cell Extrusion: A Stress-Responsive Force for Good or Evil in Epithelial Homeostasis
  • Tác giả: Ohsawa, Shizue ; Vaughen, John ; Igaki, Tatsushi
  • Chủ đề: apoptosis ; cancer ; cell competition ; cell extrusion ; development ; epithelia ; epithelial-mesenchymal transition ; morphogenesis ; tissue homeostasis
  • Là 1 phần của: Developmental cell, 2018-02, Vol.44 (3), p.284-296
  • Mô tả: Epithelial tissues robustly respond to internal and external stressors via dynamic cellular rearrangements. Cell extrusion acts as a key regulator of epithelial homeostasis by removing apoptotic cells, orchestrating morphogenesis, and mediating competitive cellular battles during tumorigenesis. Here, we delineate the diverse functions of cell extrusion during development and disease. We emphasize the expanding role for apoptotic cell extrusion in exerting morphogenetic forces, as well as the strong intersection of cell extrusion with cell competition, a homeostatic mechanism that eliminates aberrant or unfit cells. While cell competition and extrusion can exert potent, tumor-suppressive effects, dysregulation of either critical homeostatic program can fuel cancer progression. Epithelial tissues robustly respond to internal and external stressors via dynamic cellular rearrangements. Cell extrusion acts as a key regulator of epithelial homeostasis by removing apoptotic cells, orchestrating morphogenesis, and mediating competitive cellular battles during tumorigenesis. Ohsawa et al. delineate the diverse functions of cell extrusion during development and disease.
  • Nơi xuất bản: United States: Elsevier Inc
  • Ngôn ngữ: English
  • Số nhận dạng: ISSN: 1534-5807
    EISSN: 1878-1551
    DOI: 10.1016/j.devcel.2018.01.009
    PMID: 29408235
  • Nguồn: Open Access: Cell Press Free Archives
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