Elimination of oncogenic cells that regulate epithelial homeostasis in Drosophila
Elimination of oncogenic cells that regulate epithelial homeostasis in Drosophila
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DOI：
10.1111/dgd.12604
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发表时间：
2019-04
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影响因子：
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通讯作者：
Shizue Ohsawa
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作者：
Shizue Ohsawa
正常上皮组织通常通过细胞间通讯对新出现的致癌细胞施加抗致瘤压力。在果蝇上皮细胞中，当被正常细胞包围时，进化上保守的顶基极性基因（如scribble（scrib）和discs large（dlg））突变的致癌细胞克隆被积极消除。据报道，极性缺陷细胞中的c-Jun N-末端激酶（JNK）信号传导对其细胞死亡至关重要。然而，正常上皮组织对极性缺陷细胞发挥抗肿瘤作用的机制一直难以捉摸。在这里，我描述了我们在果蝇上皮细胞中的遗传研究，特别是关注周围正常上皮细胞对极性缺陷细胞出现的反应。此外，我还描述了最近的研究有关的机制，极性缺陷的细胞从组织中挤出，并讨论了未来的观点上皮细胞稳态的细胞-细胞通信的研究。
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.