| Interaction of polyunsaturated fatty acids and sodium butyrate during apoptosis in HT-29 human colon adenocarcinoma cells. | |
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MedLine Citation:
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PMID: 15309463 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: Dysregulation of the balance between cell growth and death in the colonic epithelium is associated with cancer promotion. Understanding how cell death in this self-renewing tissue is regulated and how it is influenced by interaction of specific dietary components, especially fat and fibre, could lead to improved treatment and prevention strategies for cancer. AIM OF THE STUDY: The effects of two types of polyunsaturated fatty acids (PUFAs)--arachidonic (AA, 20:4, n-6) or docosahexaenoic (DHA, 22:6, n-3)--on the response of human colon adenocarcinoma HT-29 cells to sodium butyrate (NaBt) were investigated. METHODS: The parameters reflecting cell proliferation and cell death were studied together with oxidative response, mitochondrial membrane potential (MMP) and changes of selected regulatory molecules associated with cell cycle (p27(Kip1) and p21(Cip1/WAF1)) and apoptosis (caspase-3, caspase-9, poly (ADP-ribose) polymerase--PARP, Bcl-2, Bax, Bak,Mcl-1). RESULTS: We demonstrated that pre-treatment with either AA or DHA attenuated cell cycle arrest caused by NaBt which is associated with modulation of p27(Kip1), but not p21(Cip1/WAF1) protein expression. On the other hand, PUFAs sensitised HT-29 cells to NaBt-induced apoptosis. An increased amount of floating cells and cells in the subG(0)/G(1) population was associated with increased reactive oxygen species production, lipid peroxidation, decrease of MMP, activation of caspase-3 and -9, PARP cleavage, and decrease in the expression of antiapoptotic Mcl-1 protein. The observed effects were modulated by the addition of a protein synthesis inhibitor, cycloheximide, and partially reversed by the antioxidant Trolox. CONCLUSIONS: PUFAs may have beneficial effects in the colon enhancing apoptosis induced by NaBt. Alteration of cell membrane lipid composition and potentiation of oxidative processes accompanied by changes in mitochondria followed by stimulation of apoptotic cascade components play a role in these effects. |
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Authors:
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Jirina Hofmanová; Alena Vaculová; Antonín Lojek; Alois Kozubík |
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Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't Date: 2004-03-10 |
Journal Detail:
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Title: European journal of nutrition Volume: 44 ISSN: 1436-6207 ISO Abbreviation: Eur J Nutr Publication Date: 2005 Feb |
Date Detail:
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Created Date: 2005-02-02 Completed Date: 2006-08-04 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 100888704 Medline TA: Eur J Nutr Country: Germany |
Other Details:
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Languages: eng Pagination: 40-51 Citation Subset: IM |
Affiliation:
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Laboratory of Cytokinetics, Institute of Biophysics, Academy of Sciences of the Czech Republic, Královopolská 135, 61265 Brno, Czech Republic. hofmanova@ibp.cz |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adenocarcinoma
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metabolism* Apoptosis* / drug effects Arachidonic Acid / administration & dosage Blotting, Western Butyrates / metabolism* Caspase 3 Caspase 9 Caspases / drug effects, metabolism Cell Cycle / drug effects Colonic Neoplasms / metabolism* Docosahexaenoic Acids / administration & dosage Dose-Response Relationship, Drug Fatty Acids, Unsaturated / metabolism* Flow Cytometry HT29 Cells Humans Lipid Peroxidation / drug effects Membrane Potentials / drug effects Microscopy, Fluorescence Poly(ADP-ribose) Polymerases / drug effects, metabolism Proto-Oncogene Proteins / drug effects, metabolism Reactive Oxygen Species / metabolism |
| Chemical | |
Reg. No./Substance:
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0/Butyrates; 0/Fatty Acids, Unsaturated; 0/Proto-Oncogene Proteins; 0/Reactive Oxygen Species; 25167-62-8/Docosahexaenoic Acids; 506-32-1/Arachidonic Acid; EC 2.4.2.30/Poly(ADP-ribose) Polymerases; EC 3.4.22.-/CASP3 protein, human; EC 3.4.22.-/CASP9 protein, human; EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Caspase 9; EC 3.4.22.-/Caspases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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