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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. Schema
  9. External Links
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We are analyzing https://link.springer.com/article/10.1007/s00432-024-05878-0.

Title:
Curcumin promotes ferroptosis in hepatocellular carcinoma via upregulation of ACSL4 | Journal of Cancer Research and Clinical Oncology
Description:
Background Ferroptosis, a novel iron-ion-dependent metabolic cell death mode with lipid peroxides as the main driving substrate, plays an irreplaceable role in the development and preventive treatment of hepatocellular carcinoma. Curcumin has potent pharmacological anti-tumor effects. Aim of the study We aimed to evaluate the ex vivo and in vivo cancer inhibitory activity of curcumin and its specific mechanism of action. Materials and Methods We used the hepatocellular carcinoma cell lines HepG2 and SMMC7721 to assess the direct inhibition of hepatocellular carcinoma proliferation by curcumin in vitro and a tumor xenograft model to evaluate the in vivo cancer inhibitory effect of curcumin. Results In this study, we found that ferroptosis’s inhibitors specifically reversed the curcumin-induced cell death pattern in HCC. After curcumin intervention, there was a substantial increase in MDA levels and iron ion levels, and a decrease in intracellular GSH levels. Meanwhile, the expression of GPX4 and SLC7A11 was significantly reduced at the protein levels, while ACSL4 and PTGS2 expression was significantly increased. Conclusions This study showed that curcumin significantly decreased the proliferation of HCC cells and significantly increased the sensitivity of ferroptosis. These results suggest that ACSL4 is a viable target for curcumin-induced ferroptosis in treating HCC.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Science
  • Education
  • Health & Fitness

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 5,000,019 visitors per month in the current month.
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How Does Link.springer.com Make Money? {💸}

The income method remains a mystery to us.

While profit motivates many websites, others exist to inspire, entertain, or provide valuable resources. Websites have a variety of goals. And this might be one of them. Link.springer.com might be making money, but it's not detectable how they're doing it.

Keywords {🔍}

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Topics {✒️}

activate ros/keap1/nrf2/mir-34a/ ros/keap1/nrf2/mir-34a/ pi3k/akt/gsk-3beta signaling pi3k/akt/gsk-3β signaling pi3k/akt/gsk-3β pathway ros-yap-jnk signaling pathway il-1β/nf-κb pathways modulating mir-21–5p/sox6 axis aa-coa generates pufa-looh apoptosis inhibitor z-vad-fmk ros-yap-jnk pathway jak/stat3 signaling pathway mito-tracker red cmxros mitophagy-related gene signature article download pdf long-term proliferative capacity anti-programmed cell death-1 regulating il-6/jak/stat3 dose-dependent cytotoxic effect iron-death-related diseases inhibit long-term proliferation hrp-labeled secondary antibody anti-cancer chinese medicines cystine transporter slc7a11/xct curcumin-induced cell death ferroptosis-related lipid metabolism curcumin-enhanced antitumor effects dose-dependently increase cellular degradation systems inhibits hepatocellular carcinoma curcumin-mediated cell death z-vad-fmk calcein/pi assay staining autophagy-induced ferroptosis response dose-dependent manner cell death modalities programmed cell death privacy choices/manage cookies previous article reporting regulating mir-21-5p turn effectively inhibits iron ion dependence iron ion levels ferroptosis-related proteins slc7a11 mitochondrial membrane potential iron ion metabolism tumor growth curves shuguang hospital affiliated nf-κb activity triggered mitochondrial apoptosis

Schema {🗺️}

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         headline:Curcumin promotes ferroptosis in hepatocellular carcinoma via upregulation of ACSL4
         description:Ferroptosis, a novel iron-ion-dependent metabolic cell death mode with lipid peroxides as the main driving substrate, plays an irreplaceable role in the development and preventive treatment of hepatocellular carcinoma. Curcumin has potent pharmacological anti-tumor effects. We aimed to evaluate the ex vivo and in vivo cancer inhibitory activity of curcumin and its specific mechanism of action. We used the hepatocellular carcinoma cell lines HepG2 and SMMC7721 to assess the direct inhibition of hepatocellular carcinoma proliferation by curcumin in vitro and a tumor xenograft model to evaluate the in vivo cancer inhibitory effect of curcumin. In this study, we found that ferroptosis’s inhibitors specifically reversed the curcumin-induced cell death pattern in HCC. After curcumin intervention, there was a substantial increase in MDA levels and iron ion levels, and a decrease in intracellular GSH levels. Meanwhile, the expression of GPX4 and SLC7A11 was significantly reduced at the protein levels, while ACSL4 and PTGS2 expression was significantly increased. This study showed that curcumin significantly decreased the proliferation of HCC cells and significantly increased the sensitivity of ferroptosis. These results suggest that ACSL4 is a viable target for curcumin-induced ferroptosis in treating HCC.
         datePublished:2024-09-23T00:00:00Z
         dateModified:2024-09-23T00:00:00Z
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         license:http://creativecommons.org/licenses/by/4.0/
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            Ferroptosis2
            Hepatocellular carcinoma 3
            ACSL44
            Lipid peroxidation5
            Oncology
            Cancer Research
            Internal Medicine
            Hematology
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      headline:Curcumin promotes ferroptosis in hepatocellular carcinoma via upregulation of ACSL4
      description:Ferroptosis, a novel iron-ion-dependent metabolic cell death mode with lipid peroxides as the main driving substrate, plays an irreplaceable role in the development and preventive treatment of hepatocellular carcinoma. Curcumin has potent pharmacological anti-tumor effects. We aimed to evaluate the ex vivo and in vivo cancer inhibitory activity of curcumin and its specific mechanism of action. We used the hepatocellular carcinoma cell lines HepG2 and SMMC7721 to assess the direct inhibition of hepatocellular carcinoma proliferation by curcumin in vitro and a tumor xenograft model to evaluate the in vivo cancer inhibitory effect of curcumin. In this study, we found that ferroptosis’s inhibitors specifically reversed the curcumin-induced cell death pattern in HCC. After curcumin intervention, there was a substantial increase in MDA levels and iron ion levels, and a decrease in intracellular GSH levels. Meanwhile, the expression of GPX4 and SLC7A11 was significantly reduced at the protein levels, while ACSL4 and PTGS2 expression was significantly increased. This study showed that curcumin significantly decreased the proliferation of HCC cells and significantly increased the sensitivity of ferroptosis. These results suggest that ACSL4 is a viable target for curcumin-induced ferroptosis in treating HCC.
      datePublished:2024-09-23T00:00:00Z
      dateModified:2024-09-23T00:00:00Z
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      pageEnd:14
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      keywords:
         Curcumin1
         Ferroptosis2
         Hepatocellular carcinoma 3
         ACSL44
         Lipid peroxidation5
         Oncology
         Cancer Research
         Internal Medicine
         Hematology
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      name:Shanghai University of Traditional Chinese Medicine, Shanghai, China
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      name:Key Laboratory of Liver and Kidney Diseases, Institute of Liver Diseases, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, China
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