Responsive ROS‐Augmented Prodrug Hybridization Nanoassemblies for Multidimensionally Synergitic Treatment of Hepatocellular Carcinoma in Cascade Assaults DOI Creative Commons
Ying‐Jie Zeng,

Yuening Cao,

Senmiao Ren

et al.

Advanced Science, Journal Year: 2025, Volume and Issue: unknown

Published: May 5, 2025

Abstract The rapid deterioration and progression of hepatocellular carcinoma (HCC) is intimately associated with copper ion overload, integrating the cuproptosis mechanism for treatment HCC presents a promising prospect. Nevertheless, cell death complexity renders efficient removal all cells insufficient solely relying on pathway. Herein, GSH‐responsive prodrug hybridization nanoassembly CA‐4S 2 @ES‐Cu exploited, which targets delivery ions to mitochondria via Elesclomol, contributing mitochondrial dysfunction evoking cuproptosis. Simultaneously, depletes GSH release CA‐4, disrupting microtubule function suppressing proliferation angiogenesis, realize dual attack against ion‐mediated metastasis HCC. Furthermore, both in mouse model synergistically elicit oxidative stress amplify effect activated immunogenetic initiate vigorous antitumor immune response cascade assault modality. Conclusively, multilevel synergistic penetrates limitations single therapy implements multidimensional targeted

Language: Английский

Responsive ROS‐Augmented Prodrug Hybridization Nanoassemblies for Multidimensionally Synergitic Treatment of Hepatocellular Carcinoma in Cascade Assaults DOI Creative Commons
Ying‐Jie Zeng,

Yuening Cao,

Senmiao Ren

et al.

Advanced Science, Journal Year: 2025, Volume and Issue: unknown

Published: May 5, 2025

Abstract The rapid deterioration and progression of hepatocellular carcinoma (HCC) is intimately associated with copper ion overload, integrating the cuproptosis mechanism for treatment HCC presents a promising prospect. Nevertheless, cell death complexity renders efficient removal all cells insufficient solely relying on pathway. Herein, GSH‐responsive prodrug hybridization nanoassembly CA‐4S 2 @ES‐Cu exploited, which targets delivery ions to mitochondria via Elesclomol, contributing mitochondrial dysfunction evoking cuproptosis. Simultaneously, depletes GSH release CA‐4, disrupting microtubule function suppressing proliferation angiogenesis, realize dual attack against ion‐mediated metastasis HCC. Furthermore, both in mouse model synergistically elicit oxidative stress amplify effect activated immunogenetic initiate vigorous antitumor immune response cascade assault modality. Conclusively, multilevel synergistic penetrates limitations single therapy implements multidimensional targeted

Language: Английский

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