重编程
肿瘤微环境
细胞生物学
巨噬细胞
细胞代谢
离子通道
化学
癌症研究
下调和上调
钾通道
新陈代谢
肿瘤细胞
生物
细胞
生物化学
生物物理学
体外
基因
受体
作者
Umar Al-Sheikh,Kang Lee
出处
期刊:Cell Metabolism
[Elsevier]
日期:2022-11-01
卷期号:34 (11): 1613-1615
被引量:1
标识
DOI:10.1016/j.cmet.2022.10.009
摘要
Diverse ion channels have dysregulated functional expression in the tumor microenvironment (TME). In this issue of Cell Metabolism, Chen et al. reveal that high intratumoral K+ ions restrict the plasticity of tumor-associated macrophages (TAMs). Inhibition of the Kir2.1 potassium channel induced metabolic reprogramming and repolarization of pro-tumor M2-TAMs to tumoricidal M1-like states.
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