放射增敏剂
抗辐射性
化学
放射治疗
癌症研究
伏立诺他
细胞生物学
内体
诺可达唑
纳米医学
胶质母细胞瘤
组蛋白脱乙酰基酶
乙酰肝素酶
PI3K/AKT/mTOR通路
细胞内
组织蛋白酶
肽
生物物理学
平衡
纳米纤维
DNA损伤
药物输送
作者
Xueyin Hu,Wei Cheng,Jun Che,Yuanfang Chen,Yue Shang,Cong Gao,Changfen Bi,Saijun Fan,Shuqin Li,Luntao Liu
出处
期刊:ACS Nano
[American Chemical Society]
日期:2025-12-05
卷期号:19 (50): 42436-42454
标识
DOI:10.1021/acsnano.5c15001
摘要
Glioblastoma (GBM) radiotherapy is hampered by intrinsic radioresistance. Current radiosensitizers face two unresolved hurdles: inability to dynamically traverse sequential physiological barriers of GBM and lack of multitargeted action against the pathways driving radioresistance. Here, we developed h-Pep-MTZ, a biobarrier-adaptive peptide-radiosensitizer addressing both. This system undergoes smart multistage transformations to overcome key delivery barriers: It first circulates as large, negatively charged nanoparticles to prolong plasma half-life; then converts to small, positively charged particles via tumor-overexpressed heparanase for deep tumor penetration; and finally assembles into long nanofibers triggered by lysosomal cathepsin B and acidity to extend tumor retention. Importantly, the nanofibers mechanically disrupt lysosomes, increasing lysosomal membrane permeability, inhibiting AKT activation, reducing autophagy, and impairing cytoskeletal integrity─synergistically sensitizing tumors to radiation. This strategy combined with 6 Gy radiation achieved 82.5% tumor suppression in conventional U251 models and 60.4% in radioresistant U87 models, significantly outperforming the clinical radiosensitizer sodium glycididazole. This strategy provides a paradigm for overcoming GBM radioresistance by leveraging bioresponsive nanoscale transformations and lysosomal targeting.
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