免疫监视
肝癌
癌症研究
生物
癌症
癌细胞
免疫系统
重编程
脂肪性肝炎
肿瘤微环境
脂质代谢
肿瘤进展
免疫疗法
免疫检查点
脂肪肝
免疫学
癌症干细胞
转移
癌症免疫疗法
NKG2D公司
肝再生
自然杀伤细胞
细胞
癌变
肝细胞
肝肿瘤
获得性免疫系统
肝细胞
转录组
Wnt信号通路
作者
Liang Shi,Boqiang Liu,Ruya Sun,Jing He,Hao Shen,Weiqi Li,Yi Wang,Yi Wang,Weijun Zhao,Chenqi Jin,Binghan Jin,Yuanshi Tian,Lingfeng Ma,Lidan Hou,Mingyu Chen,Jiaying Shen,Bo Shen,Xiao Liang,Hong Yu,Yifan Wang
标识
DOI:10.1038/s41467-026-74360-x
摘要
Tumor evolution enables liver cancer cells to acquire survival advantages and evade therapy-induced cell death. However, the role of natural killer (NK) cells in liver cancer evolution remains unclear. Here, we establish immune-humanized spatiotemporal liver cancer models and integrate single-cell, spatial transcriptomic, and CRISPR/Cas9 screening analyses to investigate this process. We demonstrate that early NK cell-mediated immunosurveillance promotes tumor cell state transition and impairs subsequent adaptive immune responses. Mechanistically, NK cells induce lipid metabolic reprogramming, particularly cholesterol accumulation, and enhance tumor stemness, both of which promote liver cancer evolution. Furthermore, combined anti-LAG-3 treatment and liver X receptor activation suppress tumor evolution and improve the efficacy and durability of immune checkpoint blockade in advanced liver cancer. Collectively, our findings identify that NK cell-mediated early immunosurveillance promotes liver cancer evolution and suggest immunometabolic therapy as a potential strategy for advanced liver cancer. NK cell function in liver cancer has been shown and may influence the progression of liver cancer. Here the authors use mouse liver cancer models and spatial transcriptomics in an immune-humanized liver cancer mouse model to show that NK cells can influence the early progression of liver cancer by altering lipid metabolism and tumour stemness, subsequently demonstrating that inhibition of these pathways can enhance immune cell-mediated tumour control.
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