Iron-Sulfur Clusters: A Key Factor of Regulated Cell Death in Cancer

Zhang, Mengning; Liu, Zhijun; Le, Yifei; Gu, Zhenqi; Zhao, Hong

doi:10.1155/2022/7449941

Cited by 8 publications

(5 citation statements)

References 173 publications

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“…These Fe-S clusters are instrumental in directing various programmed cell death pathways, notably in ferroptosis and cuproptosis ( Figure 1 ). Their essentiality in apoptosis and PANoptosis also highlights their influence over the mitochondrial microenvironment, further underscoring their impact on cellular death processes ( Zhang et al, 2022 ).…”

Section: Panoptosis and Other Ion-related Cell Deathmentioning

confidence: 99%

Editorial: The roles of ion-induced cell death in cancer treatment: volume II

Zhang,

He,

Thakur

et al. 2023

Front. Pharmacol.

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Section: Panoptosis and Other Ion-related Cell Deathmentioning

confidence: 99%

Editorial: The roles of ion-induced cell death in cancer treatment: volume II

Zhang,

He,

Thakur

et al. 2023

Front. Pharmacol.

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“…Tristetraprolin, expressed under iron-deficient conditions, was found to reduce the synthesis of various iron-binding proteins, especially iron-sulfur proteins, by degrading mRNA transcripts and maintaining the capacity of the cellular iron pool [ 78 ]. Furthermore, inhibition key proteins involved in the synthesis of iron-sulfur clusters, namely FXN and NSF1, can hinder the biosynthesis of said clusters, hasten the accumulation of free iron, and facilitate iron-induced cell death [ 79 ]. Upregulation of iron response element binding protein (IREB2) leads to increased synthesis of ferritin heavy and light chains of ferritin, as well as stable state of ferric ions in the steady state of ferritin [ 80 ].…”

Section: Iron Metabolism Regulationmentioning

confidence: 99%

Ferroptosis and its role in gastric and colorectal cancers

Hou,

Wang,

et al. 2024

Korean J Physiol Pharmacol

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Ferroptosis is a novel mechanism of programmed cell death, characterized by intracellular iron overload, intensified lipid peroxidation, and abnormal accumulation of reactive oxygen species, which ultimately resulting in cell membrane impairment and demise. Research has revealed that cancer cells exhibit a greater demand for iron compared to normal cells, indicating a potential susceptibility of cancer cells to ferroptosis. Stomach and colorectal cancers are common gastrointestinal malignancies, and their elevated occurrence and mortality rates render them a global health concern. Despite significant advancements in medical treatments, certain unfavorable consequences and drug resistance persist. Consequently, directing attention towards the phenomenon of ferroptosis in gastric and colorectal cancers holds promise for enhancing therapeutic efficacy. This review aims to elucidate the intricate cellular metabolism associated with ferroptosis, encompassing lipid and amino acid metabolism, as well as iron metabolic processes. Furthermore, the significance of ferroptosis in the context of gastric and colorectal cancer is thoroughly examined and discussed.

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“…ISC is an important inorganic cofactor that is widely engaged in a variety of biological functions including electron transfer which is the fundamental basis for cellular ATP production and protein synthesis. Meanwhile, recent studies have shown that ISC is tightly associated with DNA regulation ( 81 – 83 ).…”

Section: Recent Reports On Intrinsic Cellular Iron Metabolism and Fer...mentioning

confidence: 99%

Exploring the relationship between anastasis and mitochondrial ROS-mediated ferroptosis in metastatic chemoresistant cancers: a call for investigation

Cao,

Lu,

Beeraka

et al. 2024

Front. Immunol.

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Ferroptosis induces significant changes in mitochondrial morphology, including membrane condensation, volume reduction, cristae alteration, and outer membrane rupture, affecting mitochondrial function and cellular fate. Recent reports have described the intrinsic cellular iron metabolism and its intricate connection to ferroptosis, a significant kind of cell death characterized by iron dependence and oxidative stress regulation. Furthermore, updated molecular insights have elucidated the significance of mitochondria in ferroptosis and its implications in various cancers. In the context of cancer therapy, understanding the dual role of anastasis and ferroptosis in chemoresistance is crucial. Targeting the molecular pathways involved in anastasis may enhance the efficacy of ferroptosis inducers, providing a synergistic approach to overcome chemoresistance. Research into how DNA damage response (DDR) proteins, metabolic changes, and redox states interact during anastasis and ferroptosis can offer new insights into designing combinatorial therapeutic regimens against several cancers associated with stemness. These treatments could potentially inhibit anastasis while simultaneously inducing ferroptosis, thereby reducing the likelihood of cancer cells evading death and developing resistance to chemotherapy. The objective of this study is to explore the intricate interplay between anastasis, ferroptosis, EMT and chemoresistance, and immunotherapeutics to better understand their collective impact on cancer therapy outcomes. We searched public research databases including google scholar, PubMed, relemed, and the national library of medicine related to this topic. In this review, we discussed the interplay between the tricarboxylic acid cycle and glycolysis implicated in modulating ferroptosis, adding complexity to its regulatory mechanisms. Additionally, the regulatory role of reactive oxygen species (ROS) and the electron transport chain (ETC) in ferroptosis has garnered significant attention. Lipid metabolism, particularly involving GPX4 and System Xc- plays a significant role in both the progression of ferroptosis and cancer. There is a need to investigate the intricate interplay between anastasis, ferroptosis, and chemoresistance to better understand cancer therapy clinical outcomes. Integrating anastasis, and ferroptosis into strategies targeting chemoresistance and exploring its potential synergy with immunotherapy represent promising avenues for advancing chemoresistant cancer treatment. Understanding the intricate interplay among mitochondria, anastasis, ROS, and ferroptosis is vital in oncology, potentially revolutionizing personalized cancer treatment and drug development.

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Iron-Sulfur Clusters: A Key Factor of Regulated Cell Death in Cancer

Cited by 8 publications

References 173 publications

Editorial: The roles of ion-induced cell death in cancer treatment: volume II

Editorial: The roles of ion-induced cell death in cancer treatment: volume II

Ferroptosis and its role in gastric and colorectal cancers

Exploring the relationship between anastasis and mitochondrial ROS-mediated ferroptosis in metastatic chemoresistant cancers: a call for investigation

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