RNF43 p.G659fs 通过 PI3K/AKT/mTOR 信号通路和 HLA-E 上调导致 MSI-high 结直肠癌中 NK 细胞功能障碍
RNF43 p.G659fs leads to natural killer cell dysfunction in MSI-high colorectal cancer through PI3K/AKT/mTOR signaling and HLA-E up-regulation.
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
英文原题:Exercise-Induced Metabolic Reprogramming and Immune Modulation: A Novel Strategy for Cancer Therapy.
Exercise-Induced Metabolic Reprogramming and Immune Modulation: A Novel Strategy for Cancer Therapy.
分数与星级只用于站内排序 —— 不代表疗效、安全性或个人适用性。
运动代表一种能够同时调节肿瘤代谢和免疫的非药物策略。规律的身体活动可重编程全身及肿瘤局部代谢网络,包括葡萄糖、乳酸、氨基酸和脂质通路,同时增强固有免疫和适应性免疫应答。运动诱导的肌因子(如 IL-6、IL-15、irisin、SPARC)以及改善的血管化有助于重塑肿瘤微环境(TME),减轻免疫抑制性代谢物积累,并促进 T 细胞和 NK 细胞浸润。在机制上,运动激活包括 AMPK-mTOR-HIF1、PGC-1 -ERR 和 IL-6/STAT3 轴在内的整合信号网络,支持代谢灵活性和抗肿瘤免疫。转化和临床研究表明,运动可增强化疗和免疫治疗疗效,而基于 FITT 原则、生物标志物和患者特异性耐受性的精准运动处方可能最大化治疗获益。本综述总结了运动诱导代谢-免疫重编程的分子和全身机制,并概述了肿瘤学临床转化策略。
Exercise represents a non-pharmacological strategy capable of concurrently modulating tumor metabolism and immunity. Regular physical activity reprograms systemic and tumorlocalized metabolic networks, including glucose, lactate, amino acid, and lipid pathways, while enhancing innate and adaptive immune responses.
Exercise-induced myokines (e. g. , IL-6, IL-15, irisin, SPARC) and improved vascularization contribute to reshaping the tumor microenvironment (TME), mitigating immunosuppressive metabolite accumulation, and promoting T cell and NK cell infiltration.
Mechanistically, exercise activates integrated signaling networks including AMPK-mTOR-HIF1 , PGC-1 -ERR , and IL-6/STAT3 axes, supporting metabolic flexibility and anti-tumor immunity.
Translational and clinical studies suggest exercise can enhance chemotherapy and immunotherapy efficacy, while precision exercise prescriptions based on FITT principles, biomarkers, and patient-specific tolerance may maximize therapeutic benefits. This review summarizes the molecular and systemic mechanisms of exercise-induced metabolic-immune reprogramming and outlines strategies for clinical translation in oncology.
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