TRAIL and docosahexaenoic acid cooperate to induce HT-29 colon cancer cell death
Language English Country Ireland Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
16157217
DOI
10.1016/j.canlet.2004.12.016
PII: S0304-3835(04)00982-6
Knihovny.cz E-resources
- MeSH
- Adenocarcinoma pathology MeSH
- Apoptosis physiology MeSH
- Cell Adhesion MeSH
- Docosahexaenoic Acids pharmacology MeSH
- Drug Interactions MeSH
- Humans MeSH
- Membrane Glycoproteins physiology MeSH
- Tumor Cells, Cultured MeSH
- Colonic Neoplasms pathology MeSH
- TNF-Related Apoptosis-Inducing Ligand MeSH
- Apoptosis Regulatory Proteins MeSH
- Gene Expression Regulation, Neoplastic drug effects MeSH
- Tumor Necrosis Factor-alpha physiology MeSH
- Cell Survival MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Docosahexaenoic Acids MeSH
- Membrane Glycoproteins MeSH
- TNF-Related Apoptosis-Inducing Ligand MeSH
- Apoptosis Regulatory Proteins MeSH
- Tumor Necrosis Factor-alpha MeSH
- TNFSF10 protein, human MeSH Browser
The resistance of some cancer cells to TRAIL-induced apoptosis is a major obstacle in successful clinical application of this cytokine. Combination treatment with agents capable of sensitising the cells to TRAIL effects is beneficial for new cancer treatment strategies. Docosahexaenoic acid (DHA) is under intense investigation for its ability to affect cancer cell growth and apoptosis. We demonstrated a modulation of TRAIL-induced apoptosis of HT-29 human colon cancer cells by DHA on the molecular (pro-caspase-3, -8, Bid, PARP cleavage) and cellular (cell viability and adhesion) level. To conclude, TRAIL and DHA were shown to cooperate in the induction of colon cancer cell apoptosis.
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