期刊
DEVELOPMENT GROWTH & DIFFERENTIATION
卷 61, 期 5, 页码 337-342出版社
WILEY
DOI: 10.1111/dgd.12604
关键词
cell-cell communication; Drosophila; oncogenic polarity-deficient cells; tumor suppressive cell competition
资金
- Japan Foundation for Applied Enzymology
- Japan Society for the Promotion of Science [15H05862, 17H03673]
- Takeda Science Foundation
- Grants-in-Aid for Scientific Research [15H05862, 17H03673] Funding Source: KAKEN
Normal epithelial tissues often put anti-tumorigenic pressure on newly emerged oncogenic cells through cell-cell communications. In Drosophila epithelium, clones of oncogenic cells mutant for evolutionarily conserved apico-basal polarity genes such as scribble (scrib) and discs large (dlg) are actively eliminated when surrounded by normal cells. It has been reported that c-Jun N-terminal kinase (JNK) signaling in polarity-deficient cells is crucial for their cell death. However, the mechanism by which normal epithelial tissues exert anti-tumorigenic effects on polarity-deficient cells had been elusive. Here, I describe our genetic studies in Drosophila epithelium especially focused on the role of surrounding normal epithelial cells in response to the emergence of polarity-deficient cells. Furthermore, I also describe recent studies regarding the mechanism by which polarity-deficient cells are extruded from the tissue, and discuss future perspectives on the study of cell-cell communications in epithelial homeostasis.
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