Natural medicinal ingredients induce tumor ferroptosis and related mechanisms

Xuan, Zixue; ZHANG, Yiwen; Pan, Zongfu; Zheng, Xiaowei; Huang, Ping

doi:10.3724/zdxbyxb-2021-0198

Cited by 2 publications

(2 citation statements)

References 38 publications

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“…Treatment with doxorubicin significantly reduced the tumor mass composed of HCT116 (a human colon cancer cell line) cells with gpx4 knockdown compared to the control nude mice without gpx4 knockdown [ 105 ]. As an efficient inhibitor of ferroptosis, GPX4 has provided drug resistance to tumor therapies, which is a significant challenge in the clinic with novel molecular targets and therapeutic strategies [ 106 , 107 ].…”

Section: Potential Role Of Gpx4 In Cancer Therapymentioning

confidence: 99%

Prospects for Anti-Tumor Mechanism and Potential Clinical Application Based on Glutathione Peroxidase 4 Mediated Ferroptosis

Chen

Shi

Sun

et al. 2023

IJMS

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Ferroptosis, characterized by excessive iron accumulation and lipid peroxidation, is a novel form of iron-dependent cell death, which is morphologically, genetically, and biochemically distinct from other known cell death types, such as apoptosis, necrosis, and autophagy. Emerging evidence shows that glutathione peroxidase 4 (GPX4), a critical core regulator of ferroptosis, plays an essential role in protecting cells from ferroptosis by removing the product of iron-dependent lipid peroxidation. The fast-growing studies on ferroptosis in cancer have boosted a perspective on its use in cancer therapeutics. In addition, significant progress has been made in researching and developing tumor therapeutic drugs targeting GPX4 based on ferroptosis, especially in acquired drug resistance. Selenium modulates GPX4-mediated ferroptosis, and its existing form, selenocysteine (Sec), is the active center of GPX4. This review explored the structure and function of GPX4, with the overarching goal of revealing its mechanism and potential application in tumor therapy through regulating ferroptosis. A deeper understanding of the mechanism and application of GPX4-mediated ferroptosis in cancer therapy will provide new strategies for the research and development of antitumor drugs.

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Section: Potential Role Of Gpx4 In Cancer Therapymentioning

confidence: 99%

Prospects for Anti-Tumor Mechanism and Potential Clinical Application Based on Glutathione Peroxidase 4 Mediated Ferroptosis

Chen

Shi

Sun

et al. 2023

IJMS

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“…GSH is a coenzyme factor of GSH peroxidase 4 (GPx4), an essential reaction substrate for the degradation of lipid peroxides. As a key enzyme regulating ferroptosis, GPx4 can inhibit the occurrence of ferroptosis by catalyzing the reduction of lipid peroxides ( Xuan et al, 2021 ). Patients with OC have markedly low levels of superoxide dismutase, GSH peroxidase, and GSH transferase ( Sushma et al, 2021 ).…”

Section: Introductionmentioning

confidence: 99%

Network Pharmacology Identifies Therapeutic Targets and the Mechanisms of Glutathione Action in Ferroptosis Occurring in Oral Cancer

Huang

Zhan

2022

Front. Pharmacol.

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Oral cancer (OC) is one of the most pernicious cancers with increasing incidence and mortality worldwide. Surgery is the primary approach for the treatment of early-stage OC, which reduces the quality of life of the patients. Therefore, there is an urgent need to discover novel treatments for OC. Targeting ferroptosis to induce cell death through the modulation of lipid oxidation has been used as a new approach to treat many cancers. Glutathione (GSH) is a coenzyme factor of GSH peroxidase 4, and it carries potential applicability in treating OC. By using network pharmacology and molecular docking followed by systematic bioinformatic analysis, we aimed to study GSH-targeting ferroptosis to treat OC. We identified 14 core molecular targets, namely, EGFR, PTGS2, HIF1A, VEGFA, TFRC, SLC2A1, CAV1, CDKN2A, SLC3A2, IFNG, NOX4, DDIT4, CA9, and DUSP1, involved in ferroptosis that were targeted by GSH for OC treatment. Functional characterization of these molecular targets showed their importance in the control of cell apoptosis, cell proliferation, and immune responses through various kinase activities such as the mitogen-activated protein kinase activity (e.g., ERK1 and ERK2 cascades) and modulation of TOR signaling (e.g., the HIF-1 signaling pathway). Molecular docking further revealed the direct binding of GSH with EGFR, PTGS2, and HIF1A proteins. These findings provide a novel insight into the targets of GSH in ferroptosis as well as possible molecular mechanisms involved, suggesting the possible use of GSH as a combined therapy for treating OC.

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Natural medicinal ingredients induce tumor ferroptosis and related mechanisms

Cited by 2 publications

References 38 publications

Prospects for Anti-Tumor Mechanism and Potential Clinical Application Based on Glutathione Peroxidase 4 Mediated Ferroptosis

Prospects for Anti-Tumor Mechanism and Potential Clinical Application Based on Glutathione Peroxidase 4 Mediated Ferroptosis

Network Pharmacology Identifies Therapeutic Targets and the Mechanisms of Glutathione Action in Ferroptosis Occurring in Oral Cancer

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