Tumor microenvironments self-activated nanoscale metal-organic frameworks for ferroptosis based cancer chemodynamic/photothermal/chemo therapy.

Yu Liang; Li Zhang; Chao Peng; Shiyu Zhang; Siwen Chen; Xin Qian; Wanxian Luo; Qing Dan; Yongyan Ren; Yingjia LI; Bingxia Zhao

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Tumor microenvironments self-activated nanoscale metal-organic frameworks for ferroptosis based cancer chemodynamic/photothermal/chemo therapy.

Author: Yu LIANG ¹ ; Li ZHANG ¹ ; Chao PENG ¹ ; Shiyu ZHANG ¹ ; Siwen CHEN ² ; Xin QIAN ² ; Wanxian LUO ¹ ; Qing DAN ¹ ; Yongyan REN ³ ; Yingjia LI ¹ ; Bingxia ZHAO ²
Author Information

1. Department of Medicine Ultrasonics, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
2. Guangzhou Key Laboratory of Tumor Immunology Research, Cancer Research Institute, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China.
3. Central Laboratory, Southern Medical University, Guangzhou 510515, China.
Publication Type:Journal Article
Keywords: Drug delivery; Fenton reaction; Ferroptosis; GSH depletion; Metal-organic frameworks (MOFs); Tumor microenvironments
From: Acta Pharmaceutica Sinica B 2021;11(10):3231-3243
CountryChina
Language:English
Abstract: Ferroptosis, as a newly discovered cell death form, has become an attractive target for precision cancer therapy. Several ferroptosis therapy strategies based on nanotechnology have been reported by either increasing intracellular iron levels or by inhibition of glutathione (GSH)-dependent lipid hydroperoxidase glutathione peroxidase 4 (GPX4). However, the strategy by simultaneous iron delivery and GPX4 inhibition has rarely been reported. Herein, novel tumor microenvironments (TME)-activated metal-organic frameworks involving Fe & Cu ions bridged by disulfide bonds with PEGylation (FCSP MOFs) were developed, which would be degraded specifically under the redox TME, simultaneously achieving GSH-depletion induced GPX4 inactivation and releasing Fe ions to produce ROS