谷氨酰胺
癌症研究
肿瘤微环境
GPX4
化学
免疫系统
乳腺癌
癌细胞
脂质过氧化
前列腺癌
脂质代谢
谷胱甘肽
癌症
新陈代谢
代谢途径
程序性细胞死亡
细胞生物学
自噬
光动力疗法
下调和上调
脂肪酸代谢
生物化学
谷氨酰胺分解
氧化磷酸化
髓系细胞
氨基酸
医学
炎症
生物
作者
Jiayue Ding,Jingchao Liu,Liheng Liang,W. Wang,Yingchao Li,Chuanxiu Zhu,Jiayao Wen,Zhijing He,J Li,Youqi Zhang,Guangxi Zhai,Xiaoye Yang
摘要
-MIL-101(Fe)), followed by surface coating for tumor-targeting. Experimental data reveal that Ce6-based photodynamic therapy synergizes with iron-mediated Fenton reaction, potently driving lipid peroxides (LPOs) accumulation and triggering ferroptosis of 4T1 cells. Meanwhile, IMD-0354-mediated Gln metabolic intervention is proven to inhibit glutathione (GSH) synthesis and activate lipophagy, thereby increasing free fatty acids (FFA) levels as an essential "fuel" for lipid peroxidation and overcoming a key limitation in ferroptosis efficacy. Additionally, Gln metabolism inhibition attenuates immunosuppressive M2 macrophage polarization, ultimately boosting antitumor immunity. Thus, MICLM effectively induces ferroptosis and remodels the tumor immune microenvironment via amino acid metabolic intervention, offering a promising strategy for ferroptosis-based therapy.
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