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Colon cancer cell chemosensitisation by fish oil emulsion involves apoptotic mitochondria pathway

Granci, Virginie ; Cai, Fang ; Lecumberri, Elena ; Clerc, Aurélie ; Dupertuis, Yves M. ; Pichard, Claude

In: British Journal of Nutrition, 2013, vol. 109, no. 7, p. 1188-1195

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    Titre
    • Colon cancer cell chemosensitisation by fish oil emulsion involves apoptotic mitochondria pathway
    Auteur
    • Granci, Virginie. Unit of Nutrition, Geneva University Hospital, Rue Gabrielle-Perret-Gentil 4, 1211 Geneva 14, Switzerland
    • Cai, Fang. Unit of Nutrition, Geneva University Hospital, Rue Gabrielle-Perret-Gentil 4, 1211 Geneva 14, Switzerland
    • Lecumberri, Elena. Unit of Nutrition, Geneva University Hospital, Rue Gabrielle-Perret-Gentil 4, 1211 Geneva 14, Switzerland
    • Clerc, Aurélie. Unit of Nutrition, Geneva University Hospital, Rue Gabrielle-Perret-Gentil 4, 1211 Geneva 14, Switzerland
    • Dupertuis, Yves M.. Unit of Nutrition, Geneva University Hospital, Rue Gabrielle-Perret-Gentil 4, 1211 Geneva 14, Switzerland
    • Pichard, Claude. Unit of Nutrition, Geneva University Hospital, Rue Gabrielle-Perret-Gentil 4, 1211 Geneva 14, Switzerland
    Type de document
    • Postprint
    Langue
    • Anglais
    Publié dans
    • British Journal of Nutrition, 2013, vol. 109, no. 7, p. 1188-1195. Cambridge University Press
    Autre version électronique
    Identifiant OAI-PMH
    • oai:doc.rero.ch:304749
    Summary
    Adjuvant use of safe compounds with anti-tumour properties has been proposed to improve cancer chemotherapy outcome. We aimed to investigate the effects of fish oil emulsion (FOE) rich in n-3 PUFA with the standard chemotherapeutic agents 5-fluorouracil (5-FU), oxaliplatin (OX) or irinotecan (IRI) on two human colorectal adenocarcinoma cells with different genetic backgrounds. The HT-29 (Bax+/+) and LS174T (Bax−/−) cells were co-treated for 24-72h with 1μm-5-FU, 1μm-OX or 10μm-IRI and/or FOE dilution corresponding to 24μm-EPA and 20·5μm-DHA. Soyabean oil emulsion (SOE) was used as isoenergetic and isolipid control. Cell viability, apoptosis and nuclear morphological changes were evaluated by cytotoxic colorimetric assay, flow cytometry analysis with annexin V and 4′,6′-diamidino-2-phenylindole staining, respectively. A cationic fluorescent probe was used to evaluate mitochondrial dysfunction, and protein expression involved in mitochondrial apoptosis was determined by Western blot. In contrast to SOE, co-treatment with FOE enhanced significantly the pro-apoptotic and cytotoxic effects of 5-FU, OX or IRI in HT-29 but not in LS174T cells (two-way ANOVA, P<0·01). These results were confirmed by the formation of apoptotic bodies in HT-29 cells. A significant increase in mitochondrial membrane depolarisation was observed after the combination of 5-FU or IRI with FOE in HT-29 but not in LS174T cells (P<0·05). Co-administration of FOE with the standard agents, 5-FU, OX and IRI, could be a good alternative to increase the efficacy of chemotherapeutic protocols through a Bax-dependent mitochondrial pathway