Ferrocene-conjugated polymeric platform via amide bond formation facilitates enhanced in situ fenton reaction and robust immune responses in combination with toll-like receptor 7/8 agonist

Hao, Yanyun; Li, Hui; Ren, Fangfang; Feng, Ruihua; Liu, Yang; Li, Xia; Chen, Hongfei; Zou, Jing; Huang, Lingling; Zhang, Shiying; Shan, Gang; Yang, Zhijie; Zhang, Zhiyue

doi:10.1016/j.cej.2023.144909

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Chemodynamic Therapy1

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2024

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Cited by 2 publications

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“…To address this challenge, various Fenton-like reactions have been extensively studied in the context of oncology therapy, such as ferrocene (FcA), Cu + and Mn 2+ . [114][115][116] Nevertheless, the efficacy of CDT is hindered by suboptimal metabolism of hydrogen peroxide and metal ions within the tumor microenvironment. 117 To overcome this challenge, several promising strategies have been implemented to augment CDT effectiveness.…”

Section: Chemodynamic Therapymentioning

confidence: 99%

Sensitize Tumor Immunotherapy: Immunogenic Cell Death Inducing Nanosystems

Peng,

Li,

2024

IJN

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Section: Chemodynamic Therapymentioning

confidence: 99%

Sensitize Tumor Immunotherapy: Immunogenic Cell Death Inducing Nanosystems

Peng,

Li,

2024

IJN

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Tumor‐Selective Nano‐Dispatcher Enforced Cancer Immunotherapeutic Effects via Regulating Lactate Metabolism and Activating Toll‐Like Receptors

Liu,

Li,

Hao

et al. 2024

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The development of tumors relies on lactate metabolic reprogramming to facilitate their unchecked growth and evade immune surveillance. This poses a significant challenge to the efficacy of antitumor immunity. To address this, a tumor‐selective nano‐dispatcher, PIMDQ/Syro‐RNP, to enforce the immunotherapeutic effect through regulation of lactate metabolism and activation of toll‐like receptors is developed. By using the tumor‐targeting properties of c‐RGD, the system can effectively deliver monocarboxylate transporters 4 (MCT4) inhibitor (Syro) to inhibit lactate efflux in tumor cells, leading to decreased lactate levels in the tumor microenvironment (TME) and increased accumulation within tumor cells. The reduction of lactate in TME will reduce the nutritional support for regulatory T cells (Tregs) and promote the effector function of T cells. The accumulation of lactate in tumor cells will lead to tumor death due to cellular acidosis. In addition, it will also reduce the uptake of glucose by tumor cells, reduce nutrient plunder, and further weaken the inhibition of T cell function. Furthermore, the pH‐responsive release of Toll‐like receptors (TLR) 7/8 agonist IMDQ within the TME activates dendritic cells (DCs) and promotes the infiltration of T cells. These findings offer a promising approach for enhancing tumor immune response through targeted metabolic interventions.

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Ferrocene-conjugated polymeric platform via amide bond formation facilitates enhanced in situ fenton reaction and robust immune responses in combination with toll-like receptor 7/8 agonist

Cited by 2 publications

References 23 publications

Sensitize Tumor Immunotherapy: Immunogenic Cell Death Inducing Nanosystems

Sensitize Tumor Immunotherapy: Immunogenic Cell Death Inducing Nanosystems

Tumor‐Selective Nano‐Dispatcher Enforced Cancer Immunotherapeutic Effects via Regulating Lactate Metabolism and Activating Toll‐Like Receptors

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