流出
顺铂
化疗
二甲双胍
多重耐药
转移
佐剂
癌症研究
药理学
线粒体
化学
DNA损伤
细胞凋亡
抗药性
下调和上调
医学
生物
免疫学
生物化学
癌症
DNA
内科学
微生物学
基因
胰岛素
作者
Zaigang Zhou,Yu Liu,Xin Jiang,Chunjuan Zheng,Wenjuan Luo,Xinli Xiang,Xiao-Liang Qi,Jianliang Shen
标识
DOI:10.1016/j.ijbiomac.2022.10.167
摘要
Recently, it was newly revealed that the DNA damage induced by cis‑platinum (Cis-Pt) mediated chemotherapy was significantly impaired by the highly expressed programmed death ligand-1 (PD-L1) in tumor cells. Besides, the efficacy of Cis-Pt was also limited due to its severe side effects, especially enhanced drug efflux induced by multidrug resistance protein 1 (MDR-1) and increased tumor metastasis. Up to now, few drugs or carbohydrates could simultaneously solve these defects of Cis-Pt mediated chemotherapy. Here, we newly found that metformin-modified chitosan (Ch-Met) possessed ideal selective mitochondria accumulation capacity, leading to the further disrupted mitochondrial function, which then effectively inhibited the upregulated PD-L1 expression to inhibit DNA damage repair in tumor cells, as well as impaired drug efflux and lowered tumor metastasis. Therefore, it was demonstrated that Ch-Met could sensitize the chemotherapy efficacy of Cis-Pt.
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