三阴性乳腺癌
材料科学
癌症研究
多重耐药
表观遗传学
乳腺癌
生物
癌症
纳米技术
抗药性
遗传学
基因
作者
Xiaoyuan Ji,Daoxia Guo,Jia Ma,Lanying Li,Yun Yu,Chang Liu,Yanfeng Zhou,Jinli Sun,Qian Li,Nan Chen,Chunhai Fan,Haiyun Song
标识
DOI:10.1002/adma.202100949
摘要
Abstract The induced expansion of tumor‐initiating cells (T‐ICs) upon repeated exposure of tumors to chemotherapeutic drugs forms a major cause for chemoresistance and cancer metastasis. Here, a tumor‐microenvironment‐responsive hydrogel patch is designed to modulate the plasticity of T‐ICs in triple‐negative breast cancer (TNBC), which is insensitive to hormone‐ and HER2‐targeting. The on‐site formation of the hydrogel network patches tumors in a chemoresistant TNBC murine model and senses intratumoral reactive oxygen species for linker cleavage and payload release. Patch‐mediated inhibition of the histone demethylase lysine‐specific demethylase 1 (LSD1) epigenetically regulates the switch of T‐ICs from self‐renewal to differentiation, rehabilitating their chemosensitivity. Moreover, the hydrogel patch enhances tumor immunogenicity and increases T‐cell infiltration via epigenetic activation of innate immunity. A single‐dose of the hydrogel patch harboring LSD1 inhibitor and chemotherapy agent efficiently suppresses tumor growth, postsurgical relapse, and metastasis. The superior efficacy against multidrug resistance further reveals the broad applicability of epigenetic remodeling hydrogel patches.
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