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LINK . SPRINGER . COM {}

  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Link.springer.com Make Money
  6. Keywords
  7. Topics
  8. Questions
  9. Schema
  10. External Links
  11. Analytics And Tracking
  12. Libraries
  13. CDN Services

We are analyzing https://link.springer.com/article/10.1007/s00018-023-04907-4.

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.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Science
  • Health & Fitness
  • Education

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 7,642,828 visitors per month in the current month.

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How Does Link.springer.com Make Money? {💸}

We don't see any clear sign of profit-making.

While many websites aim to make money, others are created to share knowledge or showcase creativity. People build websites for various reasons. This could be one of them. Link.springer.com might be making money, but it's not detectable how they're doing it.

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?

Schema {🗺️}

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         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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      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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      dateModified:2023-08-19T00:00:00Z
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      name:Shutong Liu
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      name:Yuhao Ba
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      email:[email protected]
      name:Zaoqu Liu
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            name:The First Affiliated Hospital of Zhengzhou University
            address:
               name:Department of Interventional Radiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:Guojun Zhang
      url:http://orcid.org/0000-0003-1756-0082
      affiliation:
            name:The First Affiliated Hospital of Zhengzhou University
            address:
               name:Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
      name:Department of Ophthalmology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
      name:Department of Interventional Radiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
      name:Department of Colorectal Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
      name:Department of Interventional Radiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
      name:Department of Interventional Radiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
      name:Center of Reproductive Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
      name:Department of Interventional Radiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
      name:Department of Interventional Radiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
      name:Department of Pediatric Urology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
      name:Department of Interventional Radiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
      name:Department of Interventional Radiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
      name:Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China

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