Recent Progress in Ferroptosis Inducers for Cancer Therapy

Liang, Chunyong; Zhang, Xinglin; Yang, Mengsu; Dong, Xiaochen

doi:10.1002/adma.201904197

Cited by 1,175 publications

(941 citation statements)

References 153 publications

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“…Second, FIN56 binds to the enzyme squalene synthase, which leads to the depletion of endogenous antioxidant coenzyme Q10 (COQ10). This process enhances cell sensitivity to FIN56-induced ferroptosis 8 . The final category includes FINO2, an organic peroxide with many features in common with artemisinin, which causes ferroptosis due to a combined effect of the direct oxidation of labile iron and the inactivation of GPX4 8 .…”

Section: An Overview Of Ferroptosismentioning

confidence: 94%

“…This process enhances cell sensitivity to FIN56-induced ferroptosis 8 . The final category includes FINO2, an organic peroxide with many features in common with artemisinin, which causes ferroptosis due to a combined effect of the direct oxidation of labile iron and the inactivation of GPX4 8 . With the deepening of research on the mechanism of ferroptosis, many specific inhibitors of ferroptosis, such as ferrostatin-1 (Fer-1), liproxstatin-1 and vitamin E, have been found, in addition to iron chelators.…”

Section: An Overview Of Ferroptosismentioning

confidence: 94%

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Ferroptosis: past, present and future

et al. 2020

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Ferroptosis is a new type of cell death that was discovered in recent years and is usually accompanied by a large amount of iron accumulation and lipid peroxidation during the cell death process; the occurrence of ferroptosis is iron-dependent. Ferroptosis-inducing factors can directly or indirectly affect glutathione peroxidase through different pathways, resulting in a decrease in antioxidant capacity and accumulation of lipid reactive oxygen species (ROS) in cells, ultimately leading to oxidative cell death. Recent studies have shown that ferroptosis is closely related to the pathophysiological processes of many diseases, such as tumors, nervous system diseases, ischemia-reperfusion injury, kidney injury, and blood diseases. How to intervene in the occurrence and development of related diseases by regulating cell ferroptosis has become a hotspot and focus of etiological research and treatment, but the functional changes and specific molecular mechanisms of ferroptosis still need to be further explored. This paper systematically summarizes the latest progress in ferroptosis research, with a focus on providing references for further understanding of its pathogenesis and for proposing new targets for the treatment of related diseases. Facts Ferroptosis is a new type of programmed cell death, which occurs with iron dependence. Ferroptosis plays an important regulatory role in the occurrence and development of many diseases, such as tumors, neurological diseases, acute kidney injury, ischemia/reperfusion, etc. Activating or blocking the ferroptosis pathway to alleviate the progression of the disease, which provides a promising therapeutic strategy for many diseases. Open questions What is the relationship between ferroptosis and other types of cell death? Is it synergy or antagonism? Is iron necessary to promote the production of lipid peroxides, or can other substances take the place of iron in ferroptosis? What is the downstream regulation mechanism of iron in ferroptosis? How can ferroptosis promote the development of inflammation?

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Section: An Overview Of Ferroptosismentioning

confidence: 94%

Section: An Overview Of Ferroptosismentioning

confidence: 94%

Ferroptosis: past, present and future

et al. 2020

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“…One of the most important hallmarks of cancer is the efficient evasion of regulated cell death. Recently, ferroptosis, a new, yet potentially evolutionary ancient type of regulated necrosis which is triggered upon collapse of a lipid radical-specific antioxidant defence system was described [15] (recently also reviewed [16][17][18][19][20]). Whereas apoptosis, necroptosis and pyroptosis are all either directly dependent on caspases or inhibited by their activity (reviewed in-depth elsewhere [21]), ferroptosis seems to have evolved separately with, as of yet, very little known direct molecular cross-talk to other pathways of regulated cell death [21].…”

Section: Introductionmentioning

confidence: 99%

Ferroptosis in Cancer Cell Biology

Bebber

Müller

Clemente

et al. 2020

Cancers

261

209

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A major hallmark of cancer is successful evasion of regulated forms of cell death. Ferroptosis is a recently discovered type of regulated necrosis which, unlike apoptosis or necroptosis, is independent of caspase activity and receptor-interacting protein 1 (RIPK1) kinase activity. Instead, ferroptotic cells die following iron-dependent lipid peroxidation, a process which is antagonised by glutathione peroxidase 4 (GPX4) and ferroptosis suppressor protein 1 (FSP1). Importantly, tumour cells escaping other forms of cell death have been suggested to maintain or acquire sensitivity to ferroptosis. Therefore, therapeutic exploitation of ferroptosis in cancer has received increasing attention. Here, we systematically review current literature on ferroptosis signalling, cross-signalling to cellular metabolism in cancer and a potential role for ferroptosis in tumour suppression and tumour immunology. By summarising current findings on cell biology relevant to ferroptosis in cancer, we aim to point out new conceptual avenues for utilising ferroptosis in systemic treatment approaches for cancer.

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“…Selective induction of cancer cell death is the most effective therapy method for tumor [31]. Several literatures reported that ferroptosis, a common selective induction cell death, plays pivotal role in the process of tumorigenesis [32,33]. However, the systematic analysis of prostate cancer has yet to be elucidated.…”

Section: Discussionmentioning

confidence: 99%

Identification and validation of a ferroptosis-related genes based prognostic signature for prostate cancer

Liu

Gao

et al. 2020

Preprint

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Ferroptosis, an iron-dependent form of selective cell death, involves in the development of many cancers. However, systematic analysis of ferroptosis related genes (FRGs) in prostate cancer (PCa) remains to be clarified. In our research, we collected the mRNA expression profiles and clinical information of PCa patients from TCGA and MSKCC databases. The univariate, LASSO and multivariate Cox regression method were performed to construct prognostic signature in TCGA cohort. Seven FRGs, AKR1C3, ALOXE3, ATP5MC3, CARS1, MT1G, PTGS2, TFRC, were included to establish the risk model, which was validated in MSKCC dataset. Subsequently, we found that high risk group was strongly correlated with copy number alteration load, tumor burden mutation, immune cell infiltration, mRNAsi, immuetherapy and bicalutamide response. Finally, it was identified that overexpression of TFRC could induce proliferation and invasion in PCa cell lines in vitro. These results demonstrated that this risk model based on recurrence free survival (RFS) could accurately predict prognosis in PCa patients, suggesting that FRGs are promising prognostic biomarkers and drug target genes for PCa patients.

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Recent Progress in Ferroptosis Inducers for Cancer Therapy

Cited by 1,175 publications

References 153 publications

Ferroptosis: past, present and future

Ferroptosis: past, present and future

Ferroptosis in Cancer Cell Biology

Identification and validation of a ferroptosis-related genes based prognostic signature for prostate cancer

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