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《火中取栗:炎症驱动癌症中的细胞自主机制》

The Fire within: Cell-Autonomous Mechanisms in Inflammation-Driven Cancer.

机构信息

Laboratory of Gene Regulation and Signal Transduction, Department of Pharmacology, School of Medicine, University of California San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA; Department of Laboratory Medicine, Medical University of Vienna, Vienna 1090, Austria.

Laboratory of Gene Regulation and Signal Transduction, Department of Pharmacology, School of Medicine, University of California San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.

出版信息

Cancer Cell. 2019 May 13;35(5):714-720. doi: 10.1016/j.ccell.2019.04.001.

Abstract

Inflammatory cells are important for tumor initiation and promotion, providing cancer cells with cytokines that enhance cell proliferation and survival. Although malignant epithelial cells were traditionally considered to be on the receiving end of these microenvironmental interactions, recent studies show that epithelial cells can undergo inflammatory reprogramming on their own. Such epigenetic switches are often triggered by chronic tissue injury and play important roles in tissue repair. By converting terminally differentiated cells that harbor even a single oncogenic mutation to a less differentiated state with a higher proliferative potential, cell-autonomous inflammation is an important contributor to tumor initiation.

摘要

炎性细胞对于肿瘤的发生和促进至关重要,它们为癌细胞提供细胞因子,增强细胞增殖和存活。尽管恶性上皮细胞传统上被认为是这些微环境相互作用的接受者,但最近的研究表明,上皮细胞本身可以经历炎症重编程。这种表观遗传开关通常由慢性组织损伤触发,并在组织修复中发挥重要作用。通过将携带单个致癌突变的终末分化细胞转化为具有更高增殖潜能的低分化状态,细胞自主炎症是肿瘤发生的重要因素。

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