AI Article Synopsis
- Ferroptosis, a form of cell death driven by iron and lipid peroxides, plays a crucial role in treating liver cancer (hepatocellular carcinoma) and curcumin has strong anti-tumor properties.
- The study aimed to assess curcumin's effectiveness in inhibiting liver cancer cells both in laboratory settings and in live models, using specific cancer cell lines and tumor xenografts.
- Results showed that curcumin reduced liver cancer cell growth and induced ferroptosis by altering levels of certain biomarkers, indicating that ACSL4 could be a target for enhancing the effects of curcumin in liver cancer treatment.
Article Abstract
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.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11420324 | PMC |
| http://dx.doi.org/10.1007/s00432-024-05878-0 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Ena-bile-ing liver cancer growth.
Science
January 2025
Gastroenterology Division, Massachusetts General Hospital, Boston, MA, USA.
Bile acids differentially affect immune cell responses to liver cancer.
View Article and Find Full Text PDFBile acid synthesis impedes tumor-specific T cell responses during liver cancer.
Science
January 2025
NOMIS Center for Immunobiology and Microbial Pathogenesis, Salk Institute for Biological Studies, La Jolla, CA, USA.
The metabolic landscape of cancer greatly influences antitumor immunity, yet it remains unclear how organ-specific metabolites in the tumor microenvironment influence immunosurveillance. We found that accumulation of primary conjugated and secondary bile acids (BAs) are metabolic features of human hepatocellular carcinoma and experimental liver cancer models. Inhibiting conjugated BA synthesis in hepatocytes through deletion of the BA-conjugating enzyme bile acid-CoA:amino acid -acyltransferase (BAAT) enhanced tumor-specific T cell responses, reduced tumor growth, and sensitized tumors to anti-programmed cell death protein 1 (anti-PD-1) immunotherapy.
View Article and Find Full Text PDFResearch on the mechanism of eugenol in the treatment of liver cancer based on network pharmacology, molecular docking technology, and in vitro experiments.
Anticancer Drugs
January 2025
School of Clinical Medicine, Guizhou Medical University, Guiyang City, Guizhou, China.
Eugenol, a phenolic natural product with diverse pharmacological activities, remains unexplored in liver cancer. Using network pharmacology, we investigated eugenol's therapeutic mechanisms in liver cancer. We obtained eugenol's molecular structure from PubChem and screened its targets using similarity ensemble approach in Swiss Target Predictiondatabases.
View Article and Find Full Text PDFHAIC plus lenvatinib and tislelizumab for advanced hepatocellular carcinoma with Vp4 portal vein invasion.
Hepatol Int
January 2025
Department of Interventional Radiology, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, 510062, China.
Background/objective: The treatment strategy for hepatocellular carcinoma (HCC) with Vp4 (main trunk) portal vein tumor thrombosis (PVTT) remains controversial due to the dismal prognosis. We aimed to investigate the efficacy and safety of hepatic arterial infusion chemotherapy (HAIC) plus lenvatinib and tislelizumab in these patients.
Methods: This multicenter retrospective study included treatment-naive HCC patients with Vp4 PVTT from 2017 to 2022.
Temporal trends and patterns for early- and late-onset adult liver cancer incidence vary by race/ethnicity, subsite, and histologic type in the United States from 2000 to 2019.
Cancer Causes Control
January 2025
Epidemiology Department, College of Public Health, University of Nebraska Medical Center, Omaha, NE, 68198, USA.
Purpose: To examine incidence trends and patterns for early- and late-onset liver cancer.
Methods: Liver and intrahepatic bile duct (IBD) cancers diagnosed between 2000 and 2019 were acquired from 22 SEER registries. Variables included early-onset (20-49) vs.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!