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Title:
Ferroptosis and EMT: key targets for combating cancer progression and therapy resistance | Cellular and Molecular Life Sciences
Description:
Iron-dependent lipid peroxidation causes ferroptosis, a form of regulated cell death. Crucial steps in the formation of ferroptosis include the accumulation of ferrous ions (Fe2+) and lipid peroxidation, of which are controlled by glutathione peroxidase 4 (GPX4). Its crucial role in stopping the spread of cancer has been shown by numerous studies undertaken in the last ten years. Epithelial–mesenchymal transition (EMT) is the process by which epithelial cells acquire mesenchymal characteristics. EMT is connected to carcinogenesis, invasiveness, metastasis, and therapeutic resistance in cancer. It is controlled by a range of internal and external signals and changes the phenotype from epithelial to mesenchymal like. Studies have shown that mesenchymal cancer cells tend to be more ferroptotic than their epithelial counterparts. Drug-resistant cancer cells are more easily killed by inducers of ferroptosis when they undergo EMT. Therefore, understanding the interaction between ferroptosis and EMT will help identify novel cancer treatment targets. In-depth discussion is given to the regulation of ferroptosis, the potential application of EMT in the treatment of cancer, and the relationships between ferroptosis, EMT, and signaling pathways associated with tumors. Invasion, metastasis, and inflammation in cancer all include ferroptosis and EMT. The goal of this review is to provide suggestions for future research and practical guidance for applying ferroptosis and EMT in clinical practice.
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Keywords {🔍}
pubmed, ferroptosis, cancer, google, scholar, cells, cas, emt, central, cell, tumor, metastasis, iron, expression, gpx, transition, signaling, lipid, pathway, tgfβ, epithelialmesenchymal, inflammation, therapy, fig, transcription, growth, biol, mesenchymal, activation, notch, peroxidation, invasion, factor, promotes, death, epithelial, therapeutic, mechanisms, slca, mol, role, pathways, inhibits, ras, zeb, hifα, tumors, factors, inflammatory, ferritin,
Topics {✒️}
e-cadherin-nf2-hippo-yap pathway typically tgf-β-induced epithelial–mesenchymal transition /β-catenin/pparγ signaling pathway ras/raf/mek/erk pathway acute t-lymphocytic leukemia/lymphoma zhaokai zhou invasion-metastasis-cascade systemic biomarkering suppressing tgf-β/smad signaling e-cad e-cadherin shuang chen kras-induced lung adenocarcinoma e-cadherin-mediated cell kras-mutant lung adenocarcinoma cancer-acquired drug resistance e-cadherin repressors zeb1 inhibiting epithelial–mesenchymal transformation view gnotobiotic piglets colonized/infected macrophage-dependent transendothelial migration pparα-mediated lipid remodeling double-negative feedback loop small-cell lung cancer α4 integrin-expressing melanoma tgf-β reduces mir-200 gcl glutamate-cysteine ligase glutamate-cysteine ligase inhibitors pediatric high-grade glioma tgf-β1 induces emt apical-basal polar cells lowering e-cadherin expression peroxisome-ether phospholipid axis ncoa4-mediated ferritinophagy degradation renal clear-cell carcinoma tgf-β orchestrates fibrogenic injury-related molecular pattern e-cadherin expression decreases subsequent mesenchymal-epithelial transition hypoxia-induced lipid drop dose-dependently inactivates gpx4 druggable copper-signalling pathway cystine/glutamate anti-transporter tgf-β-induced emt g6pd glucose-6-phosphate dehydrogenase inhibiting tgf-induced emt xc-cystine/glutamate antiporter anti-cancer immune response xct/slc7a11 dependent manner inducing post-translational modifications reduce erastin-induced ferroptosis article download pdf
Questions {❓}
- Alba J et al (2022) Could inhibition of metalloproteinases be used to block the process of metastasis?
- Feng H, Stockwell BR (2018) Unsolved mysteries: How does lipid peroxidation cause ferroptosis?
- How can ferroptosis, therefore, result in inflammation?
- What role does ferroptosis play in the anti-inflammatory effects?
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headline:Ferroptosis and EMT: key targets for combating cancer progression and therapy resistance
description:Iron-dependent lipid peroxidation causes ferroptosis, a form of regulated cell death. Crucial steps in the formation of ferroptosis include the accumulation of ferrous ions (Fe2+) and lipid peroxidation, of which are controlled by glutathione peroxidase 4 (GPX4). Its crucial role in stopping the spread of cancer has been shown by numerous studies undertaken in the last ten years. Epithelial–mesenchymal transition (EMT) is the process by which epithelial cells acquire mesenchymal characteristics. EMT is connected to carcinogenesis, invasiveness, metastasis, and therapeutic resistance in cancer. It is controlled by a range of internal and external signals and changes the phenotype from epithelial to mesenchymal like. Studies have shown that mesenchymal cancer cells tend to be more ferroptotic than their epithelial counterparts. Drug-resistant cancer cells are more easily killed by inducers of ferroptosis when they undergo EMT. Therefore, understanding the interaction between ferroptosis and EMT will help identify novel cancer treatment targets. In-depth discussion is given to the regulation of ferroptosis, the potential application of EMT in the treatment of cancer, and the relationships between ferroptosis, EMT, and signaling pathways associated with tumors. Invasion, metastasis, and inflammation in cancer all include ferroptosis and EMT. The goal of this review is to provide suggestions for future research and practical guidance for applying ferroptosis and EMT in clinical practice.
datePublished:2023-08-19T00:00:00Z
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Metastasis
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Therapy resistance
Cell Biology
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headline:Ferroptosis and EMT: key targets for combating cancer progression and therapy resistance
description:Iron-dependent lipid peroxidation causes ferroptosis, a form of regulated cell death. Crucial steps in the formation of ferroptosis include the accumulation of ferrous ions (Fe2+) and lipid peroxidation, of which are controlled by glutathione peroxidase 4 (GPX4). Its crucial role in stopping the spread of cancer has been shown by numerous studies undertaken in the last ten years. Epithelial–mesenchymal transition (EMT) is the process by which epithelial cells acquire mesenchymal characteristics. EMT is connected to carcinogenesis, invasiveness, metastasis, and therapeutic resistance in cancer. It is controlled by a range of internal and external signals and changes the phenotype from epithelial to mesenchymal like. Studies have shown that mesenchymal cancer cells tend to be more ferroptotic than their epithelial counterparts. Drug-resistant cancer cells are more easily killed by inducers of ferroptosis when they undergo EMT. Therefore, understanding the interaction between ferroptosis and EMT will help identify novel cancer treatment targets. In-depth discussion is given to the regulation of ferroptosis, the potential application of EMT in the treatment of cancer, and the relationships between ferroptosis, EMT, and signaling pathways associated with tumors. Invasion, metastasis, and inflammation in cancer all include ferroptosis and EMT. The goal of this review is to provide suggestions for future research and practical guidance for applying ferroptosis and EMT in clinical practice.
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Metastasis
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Therapy resistance
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general
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Biochemistry
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