ArticleMarine drugs2020
Fucoidan Induces Apoptosis of HT-29 Cells via the Activation of DR4 and Mitochondrial Pathway.
Article in Marine drugs, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
10 citing papers in PubMed, 31 citations in OpenAlex.
- Fucoidan-Based Combination Strategies in Cancer Therapy: Biological Basis, Current Evidence, and Future Perspectives.International journal of molecular sciences · 2026Review
- Natural polysaccharides targeting mitochondrial function for colorectal cancer prevention and treatment: mechanisms and nano-delivery strategies.Chinese medicine · 2026Review
- Selective antimicrobial potential of fucoidans against the pathogenFrontiers in microbiology · 2026Article
- Article
- Review
- Natural Marine Products: Anti-Colorectal Cancer In Vitro and In Vivo.Marine drugs · 2022Review
- Article
- Anticancer Activity of Fucoidan via Apoptosis and Cell Cycle Arrest on Cholangiocarcinoma Cell.Asian Pacific journal of cancer prevention : APJCP · 2021Article
- The Structural Characteristics of Seaweed Polysaccharides and Their Application in Gel Drug Delivery Systems.Marine drugs · 2020Review
- Anti-Colorectal Cancer Effects of Fucoidan Complex-Based Functional Beverage Through Retarding Proliferation, Cell Cycle and Epithelial-Mesenchymal Transition Signaling Pathways.Integrative cancer therapiesArticle
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fucoidan has a variety of pharmacological activities, but the understanding of the mechanism of fucoidan-induced apoptosis of colorectal cancer cells remains limited. The results of the present study demonstrated that the JNK signaling pathway is involved in the activation of apoptosis in colorectal cancer-derived HT-29 cells, and fucoidan induces apoptosis by activation of the DR4 at the transcriptional and protein levels. The survival rate of HT-29 cells was approximately 40% in the presence of 800 μg/mL of fucoidan, but was increased to 70% after DR4 was silenced by siRNA. Additionally, fucoidan has been shown to reduce the mitochondrial membrane potential and destroy the integrity of mitochondrial membrane. In the presence of an inhibitor of cytochrome C inhibitor and DR4 siRNA or the presence of cytochrome C inhibitor only, the cell survival rate was significantly higher than when cells were treated with DR4 siRNA only. These data indicate that both the DR4 and the mitochondrial pathways contribute to fucoidan-induced apoptosis of HT-29 cells, and the extrinsic pathway is upstream of the intrinsic pathway. In conclusion, the current work identified the mechanism of fucoidan-induced apoptosis and provided a novel theoretical basis for the future development of clinical applications of fucoidan as a drug.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.