生物
肿瘤微环境
免疫系统
表观遗传学
趋化因子
转移
人口
利基
癌症研究
先天免疫系统
肿瘤异质性
癌症的体细胞进化
转录组
炎症
基因沉默
细胞迁移
免疫学
进化动力学
癌症
肺
CX3CR1型
免疫疗法
干细胞
癌细胞
组织向性
细胞
作者
Yun‐Fan Sun,Yu Zhong,Shang Liu,Shang Liu,Zefan Zhang,Chunqing Wang,Yang Liu,Junbing Chen,Xiaoying Gu,Xiaoying Gu,Keqiang Rao,Zifei Wang,Muzi Cao,Yue Wang,Waidong Huang,Xuanxuan Zou,Xi Chen,Shuangjian Qiu,Ying–Hong Shi,Hui‐Chuan Sun
出处
期刊:Science
[American Association for the Advancement of Science]
日期:2026-07-30
卷期号:393 (6810): eadz7928-eadz7928
标识
DOI:10.1126/science.adz7928
摘要
The mechanisms underlying the interactions between disseminated tumor cells (DTCs) and their tissue microenvironment during metastatic colonization are currently poorly understood. We integrated multimodal single-cell and spatial profiling from liver cancer mouse models and human metastases to track the spatiotemporal dynamics of DTCs and their microenvironments from single-cell seeding to overt lung metastasis. We identified a residual population of quiescent Phgdh high DTCs that survived initial innate immune clearance and became transiently enriched in micrometastases. These cells shaped an immune-scarce microenvironment through PHGDH-dependent, H3K27me3-mediated epigenetic silencing of chemokine transcription, thereby promoting metastatic expansion. Cx3cr1 high interstitial macrophages were also transiently enriched before DTC expansion, creating an immune-privileged niche for metastatic outgrowth by recruiting immunosuppressive cells. Inactivating the PHGDH-H3K27me3 axis in DTCs or depleting interstitial macrophages restored immune surveillance and inhibited metastatic colonization. These findings provide insights into the development of micrometastasis-targeting regimens.
科研通智能强力驱动
Strongly Powered by AbleSci AI