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干细胞谱系异常驱动伤口修复与癌症发生。

Stem Cell Lineage Infidelity Drives Wound Repair and Cancer.

作者信息

Ge Yejing, Gomez Nicholas C, Adam Rene C, Nikolova Maria, Yang Hanseul, Verma Akanksha, Lu Catherine Pei-Ju, Polak Lisa, Yuan Shaopeng, Elemento Olivier, Fuchs Elaine

机构信息

Robin Neustein Laboratory of Mammalian Development and Cell Biology, Howard Hughes Medical Institute, The Rockefeller University, New York, NY 10065, USA.

Department of Physiology and Biophysics, Institute for Computational Biomedicine, Weill Cornell Medicine, New York, NY 10065, USA.

出版信息

Cell. 2017 May 4;169(4):636-650.e14. doi: 10.1016/j.cell.2017.03.042. Epub 2017 Apr 20.

Abstract

Tissue stem cells contribute to tissue regeneration and wound repair through cellular programs that can be hijacked by cancer cells. Here, we investigate such a phenomenon in skin, where during homeostasis, stem cells of the epidermis and hair follicle fuel their respective tissues. We find that breakdown of stem cell lineage confinement-granting privileges associated with both fates-is not only hallmark but also functional in cancer development. We show that lineage plasticity is critical in wound repair, where it operates transiently to redirect fates. Investigating mechanism, we discover that irrespective of cellular origin, lineage infidelity occurs in wounding when stress-responsive enhancers become activated and override homeostatic enhancers that govern lineage specificity. In cancer, stress-responsive transcription factor levels rise, causing lineage commanders to reach excess. When lineage and stress factors collaborate, they activate oncogenic enhancers that distinguish cancers from wounds.

摘要

组织干细胞通过可能被癌细胞劫持的细胞程序促进组织再生和伤口修复。在此,我们研究皮肤中的这种现象,在稳态期间,表皮和毛囊的干细胞为各自的组织提供支持。我们发现,干细胞谱系限制的打破——赋予与这两种命运相关的特权——不仅是癌症发展的标志,而且在其中发挥作用。我们表明,谱系可塑性在伤口修复中至关重要,它在伤口修复过程中短暂发挥作用以重新引导细胞命运。在研究机制时,我们发现,无论细胞来源如何,在伤口形成时,当应激反应增强子被激活并取代控制谱系特异性的稳态增强子时,就会发生谱系不忠。在癌症中,应激反应转录因子水平升高,导致谱系调控因子过量。当谱系和应激因素协同作用时,它们会激活致癌增强子,从而将癌症与伤口区分开来。

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