Cancer cell and macrophage cross-talk in the tumor microenvironment
Cancer cell and macrophage cross-talk in the tumor microenvironment
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DOI：
10.1016/j.coph.2017.04.007
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发表时间：
2017-08-01
影响因子：
4
通讯作者：
Bruenet, Bernhard
中科院分区：
文献类型：
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作者：
Dehnel, Nathalie;Moral, Javier;Bruenet, Bernhard
肿瘤由肿瘤细胞、非恶性细胞和血管系统组成。其中之一是通过细胞-细胞接触依赖机制和/或可溶性信使进行的强烈通信。在肿瘤微环境中，细胞通常面临一定程度的氧气和营养剥夺。低氧应激改变了肿瘤细胞的代谢，但也改变了巨噬细胞的代谢，巨噬细胞是大多数实体瘤中的主要免疫细胞群体之一，随后微环境发生了变化。这改变了巨噬细胞的表型和代谢，以诱导促肿瘤重编程。营养压力也会引发自噬，以保证细胞存活，或者如果不堪重负，则退出细胞死亡。肿瘤细胞的死亡被证明是一个吸引巨噬细胞并指导其表型的通信系统。取决于肿瘤细胞死亡的模式，巨噬细胞极化的范围从促炎性活化的极端到炎症/免疫抑制性活化。在这里，我们讨论了缺氧和细胞死亡如何增加癌细胞和巨噬细胞之间的串扰。
Tumors are composed of tumor cells, nonmalignant cells, and the vascular system. Among them is intense communication via cell-cell contact-dependent mechanisms and/or soluble messengers. In the tumor microenvironment cells often face a certain degree of oxygen and nutrient deprivation. Hypoxic stress alters the metabolism of tumor cells but also of macrophages, as one dominating immune cell population in most solid tumors, with subsequent changes in the microenvironment. This alters the phenotype and metabolism of macrophages, to induce a tumor-promoting reprogramming. Nutrient stress also provokes autophagy to guarantee cell survival or, if overwhelmed, to exit toward cell demise. Death of tumor cells turned out as a communicative system attracting macrophages and directing their phenotype. Depending on the mode of tumor cell death macrophage polarization ranges from the extremes of pro-inflammatory activation toward antiinflammatory/immuno-suppressive activation. Here we discuss how hypoxia and cell death adds the cross-talk between cancer cells and macrophages.