串扰
生物
癌症
癌细胞
重编程
细胞生物学
肿瘤微环境
线粒体
代谢组学
神经科学
新陈代谢
脂质代谢
代谢网络
细胞器
代谢途径
营养感应
癌症研究
自噬
舱室(船)
氧化磷酸化
表观遗传学
生物信息学
神经系统
中枢神经系统
神经干细胞
生物神经网络
神经可塑性
生物发生
细胞代谢
粒体自噬
恶性肿瘤
癌变
作者
Songhui Shin,Shin Soo Myoung,Hye Jin Cho,Seong-Jun Kim,Namgyu Lee,Sung Jin Park
标识
DOI:10.1016/j.trecan.2025.11.006
摘要
Tumors dynamically interact with the central and peripheral nervous systems, hijacking neural plasticity and reprogramming metabolism in a bidirectional manner to drive cancer progression. Neural inputs reshape the metabolism of cancer cells and their microenvironment - glycolysis, oxidative phosphorylation, and lipid metabolism - while tumors exploit neuronal nutrients and mitochondria to thrive under metabolic stress. This review explores neurocancer metabolic crosstalk through multiple mechanisms by three principal modes of interaction, highlighting how targeting these metabolic interdependencies could disrupt tumor progression. By integrating cancer metabolism and neuroscience, it offers a conceptual framework for understanding neural-tumor metabolic circuits in malignancy and identifies potential therapeutic vulnerabilities.
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