Advanced nanomedicines for the regulation of cancer metabolism

Yang, Jiaying; Zhao, Yu; Zhou, Yanyan; Wei, Xiaolu; Wang, Hongjie; Si, Nan; Yang, Jian; Zhao, Qinghe; Bian, Baolin; Zhao, Haiyu

doi:10.1016/j.biomaterials.2022.121565

Cited by 16 publications

(19 citation statements)

References 166 publications

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“…4(a) and 4(b), the tumor cells without any treatment displayed relatively strong green fluorescence, while cells incubated with PN-CeO 2 exhibited significant decrease in the levels of the intracellular ROS in a dosedependent manner, demonstrating the ROS-scavenging ability of PN-CeO 2 . Furthermore, the quantitative analyses of the ROS levels Based on increasing knowledge of cancer biology and its altered redox status, researchers have explored numerous tumor therapy strategies, including chemotherapy, radiotherapy, photodynamic therapy, and chemodynamic therapy [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18]. Most of these tend to enhance the generation of intracellular or exogenous ROS and interfere with antioxidant defenses.…”

Section: Mechanisms Of Autophagy Inhibition By Pn-ceomentioning

confidence: 99%

“…The generation of reactive oxygen species (ROS) and subsequent oxidative damage in a tumor environment (TME) is the dominant mechanism of contemporary tumor treatment strategies, including chemotherapy [1][2][3][4], radiotherapy [5], photodynamic therapy [6,7], and photothermal and catalytic therapy [8][9][10][11][12][13][14][15][16][17][18]. However, elevated intratumoral ROS levels can also increase tumor cell survival and proliferation, especially through the activation of protective autophagy [19,20].…”

Section: Introductionmentioning

confidence: 99%

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Reductive damage induced autophagy inhibition for tumor therapy

Wang

Huang

et al. 2022

Nano Res.

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Numerous therapeutic anti-tumor strategies have been developed in recent decades. However, their therapeutic efficacy is reduced by the intrinsic protective autophagy of tumors. Autophagy plays a key role in tumorigenesis and tumor treatment, in which the overproduction of reactive oxygen species (ROS) is recognized as the direct cause of protective autophagy. Only a few molecules have been employed as autophagy inhibitors in tumor therapy to reduce protective autophagy. Among them, hydroxychloroquine is the most commonly used autophagy inhibitor in clinics, but it is severely limited by its high therapeutic dose, significant toxicity, poor reversal efficacy, and nonspecific action. Herein, we demonstrate a reductive-damage strategy to enable tumor therapy by the inhibition of protective autophagy via the catalytic scavenging of ROS using porous nanorods of ceria (PN-CeO 2 ) nanozymes as autophagy inhibitor. The antineoplastic effects of PN-CeO 2 were mediated by its high reductive activity for intratumoral ROS degradation, thereby inhibiting protective autophagy and activating apoptosis by suppressing the activities of phosphatidylinositide 3-kinase/protein kinase B and p38 mitogen-activated protein kinase pathways in human cutaneous squamous cell carcinoma. Further investigation highlighted PN-CeO 2 as a safe and efficient anti-tumor autophagy inhibitor. Overall, this study presents a reductive-damage strategy as a promising anti-tumor approach that catalytically inhibits autophagy and activates the intrinsic antioxidant pathways of tumor cells and also shows its potential for the therapy of other autophagy-related diseases. Electronic Supplementary Material Supplementary material (cellular uptake of PN-CeO 2 , effects of PN-CeO 2 on several common malignant tumor models, viability of HaCaT cells treated with PN-CeO 2 at different concentrations, time-dependent body-weight curves of SCL-1 tumor-bearing nude mice, the biodistribution of Ce element in main tissues and tumors after injection of PN-CeO 2 , measurement of Ce element concentration in urine and feces samples, H&E-stained images of main organs, and measurement of liver and kidney function in mice after different treatment) is available in the online version of this article at 10.1007/s12274-022-5139-z.

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Section: Mechanisms Of Autophagy Inhibition By Pn-ceomentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Reductive damage induced autophagy inhibition for tumor therapy

Wang

Huang

et al. 2022

Nano Res.

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“…Recently, nanomedicine-based therapeutic approaches represent viable options for early diagnosis and treatment of chronic diseases, including cancer and cardiovascular, neurological, and metabolic disorders. − Nanostructures of transition metal dichalcogenides (TMDs), as promising graphene-analogue materials, have attracted great attention due to their distinctive physio-chemical features. In particular, MoS 2 nanostructures as biologically friendly materials displayed much lower toxicity than graphene and its other analogues, more surface defect sites, and better water solubility, allowing them long-term intracellular residence via covalent Mo–S bonds. , A growing focus has been placed on exploring the potential of MoS 2 -based nanoagents to prevent and improve chronic diseases, including senescence and degenerative and cardiovascular diseases. − Accumulating data has shown that MoS 2 -based nanoagents behave as potential inhibitors for endothelial and degenerative disorders by eliminating oxidative damage, − , blocking endothelial-to-mesenchymal transition (EndMT), triggering autophagic process, and preventing amyloidogenesis. , However, it should be noted that the effect of MoS 2 quantum dots (QD) on endothelial barrier and macrophage activation, early atherosclerotic events for evaluating their potential as AS nanomedicines, has not been yet studied.…”

Section: Introductionmentioning

confidence: 99%

MoS₂ Quantum Dots Alter Macrophage Plasticity and Induce Mitophagy to Attenuate Endothelial Barrier Dysfunctions

Liu

et al. 2023

ACS Appl. Nano Mater.

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Molybdenum disulfide (MoS2), as a member of transition metal dichalcogenides (TMDs), presents enormous potential in biomedical applications due to its unique chemical–physical properties, photo-electronic properties, and biocompatibility. MoS2 nanostructures have recently been shown to be multifunctional nanotheranostic agents for neuroprotection and maintenance of endothelial homeostasis. However, whether ultrasmall MoS2 quantum dots (QD) participate in preventing the impairment of the endothelial barrier elicited by pro-inflammatory stimuli and the associated underlying mechanisms remain elusive yet. Herein, we set out to explore the protective effects of MoS2 QD on inflammatory endothelial barrier dysfunction and macrophage plasticity. We revealed an inhibitory effect of MoS2 QD on endothelial barrier impairment and monocyte–endothelial cell interactions, including monocyte adhesion and transmigration, and this might be associated with a reduced activation of focal adhesion kinase (FAK). Importantly, using an in vitro macrophage polarization system, we revealed that MoS2 QD altered macrophage plasticity via inhibiting M1-macrophage polarization, and the reduction in nuclear factor-κB (NF-κB) activation and promotion of mitophagy by MoS2 QD was involved in preventing M1 macrophage polarization. Taken together, these findings suggested potential therapeutic applications of MoS2-based bioactive nanoagents to attenuate inflammatory endothelial barrier dysfunctions that are provoked by macrophage-mediated endothelial activation.

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“…Glycolysis produces ATP very fast, 100 times faster than OXPHOS ( Locasale and Cantley, 2010 ). Tumor cells use glycolysis to accelerate energy acquisition through metabolic reprogramming to support the rapid proliferation of tumor cells ( Yang et al, 2022 ).…”

Section: Introductionmentioning

confidence: 99%

Schisantherin A inhibits cell proliferation by regulating glucose metabolism pathway in hepatocellular carcinoma

Feng

Pan

et al. 2022

Front. Pharmacol.

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Schisantherin A (STA) is a traditional Chinese medicine extracted from the plant Schisandra chinensis, which has a wide range of anti-inflammatory, antioxidant, and other pharmacological effects. This study investigates the anti-hepatocellular carcinoma effects of STA and the underlying mechanisms. STA significantly inhibits the proliferation and migration of Hep3B and HCCLM3 cells in vitro in a concentration-dependent manner. RNA-sequencing showed that 77 genes are upregulated and 136 genes are downregulated in STA-treated cells compared with untreated cells. KEGG pathway analysis showed significant enrichment in galactose metabolism as well as in fructose and mannose metabolism. Further gas chromatography-mass spectrometric analysis (GC-MS) confirmed this, indicating that STA significantly inhibits the glucose metabolism pathway of Hep3B cells. Tumor xenograft in nude mice showed that STA has a significant inhibitory effect on tumor growth in vivo. In conclusion, our results indicate that STA can inhibit cell proliferation by regulating glucose metabolism, with subsequent anti-tumor effects, and has the potential to be a candidate drug for the treatment of liver cancer.

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Advanced nanomedicines for the regulation of cancer metabolism

Cited by 16 publications

References 166 publications

Reductive damage induced autophagy inhibition for tumor therapy

Reductive damage induced autophagy inhibition for tumor therapy

MoS₂ Quantum Dots Alter Macrophage Plasticity and Induce Mitophagy to Attenuate Endothelial Barrier Dysfunctions

Schisantherin A inhibits cell proliferation by regulating glucose metabolism pathway in hepatocellular carcinoma

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Advanced nanomedicines for the regulation of cancer metabolism

Cited by 16 publications

References 166 publications

Reductive damage induced autophagy inhibition for tumor therapy

Reductive damage induced autophagy inhibition for tumor therapy

MoS2 Quantum Dots Alter Macrophage Plasticity and Induce Mitophagy to Attenuate Endothelial Barrier Dysfunctions

Schisantherin A inhibits cell proliferation by regulating glucose metabolism pathway in hepatocellular carcinoma

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MoS₂ Quantum Dots Alter Macrophage Plasticity and Induce Mitophagy to Attenuate Endothelial Barrier Dysfunctions