Dietary fatty acids specifically modulate phospholipid pattern in colon cells with distinct differentiation capacities
Jazyk angličtina Země Německo Médium print-electronic
Typ dokumentu časopisecké články
PubMed
26983609
DOI
10.1007/s00394-016-1196-y
PII: 10.1007/s00394-016-1196-y
Knihovny.cz E-zdroje
- Klíčová slova
- Apoptosis, Butyrate, Cardiolipins, Colon cancer, Docosahexaenoic acid, Phospholipids,
- MeSH
- apoptóza účinky léků MeSH
- buněčná diferenciace účinky léků MeSH
- fosfolipidy chemie MeSH
- HCT116 buňky MeSH
- kaspasa 3 genetika metabolismus MeSH
- kolon cytologie účinky léků MeSH
- kyselina máselná farmakologie MeSH
- kyseliny dokosahexaenové farmakologie MeSH
- lidé MeSH
- nádorové buněčné linie MeSH
- proliferace buněk účinky léků MeSH
- tandemová hmotnostní spektrometrie MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- CASP3 protein, human MeSH Prohlížeč
- fosfolipidy MeSH
- kaspasa 3 MeSH
- kyselina máselná MeSH
- kyseliny dokosahexaenové MeSH
PURPOSE: Although beneficial effects of the dietary n-3 docosahexaenoic acid (DHA) or butyrate in colon carcinogenesis have been implicated, the mechanisms of their action are not fully clear. Here, we investigated modulations of composition of individual phospholipid (PL) classes, with a particular emphasis on cardiolipins (CLs), in colon cells treated with DHA, sodium butyrate (NaBt), or their combination (DHA/NaBt), and we evaluated possible associations between lipid changes and cell fate after fatty acid treatment. METHODS: In two distinct human colon cell models, foetal colon (FHC) and adenocarcinoma (HCT-116) cells, we compared patterns and composition of individual PL classes following the fatty acid treatment by HPLC-MS/MS. In parallel, we measured the parameters reflecting cell proliferation, differentiation and death. RESULTS: In FHC cells, NaBt induced primarily differentiation, while co-treatment with DHA shifted their response towards cell death. In contrast, NaBt induced apoptosis in HCT-116 cells, which was not further affected by DHA. DHA was incorporated in all main PL types, increasing their unsaturation, while NaBt did not additionally modulate these effects in either cell model. Nevertheless, we identified an unusually wide range of CL species to be highly increased by NaBt and particularly by DHA/NaBt, and these effects were more pronounced in HCT-116 cells. DHA and DHA/NaBt enhanced levels of high molecular weight and more unsaturated CL species, containing DHA, which was specific for either differentiation or apoptotic responses. CONCLUSIONS: We identified a wide range of CL species in the colon cells which composition was significantly modified after DHA and NaBt treatment. These specific CL modulations might contribute to distinct cellular differentiation or apoptotic responses.
Department of Experimental Biology Faculty of Science Masaryk University Brno Czech Republic
Institute of Biostatistics and Analyses Masaryk University Brno Czech Republic
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J Nutr Biochem. 2007 Nov;18(11):736-45 PubMed
Arch Biochem Biophys. 1999 Aug 1;368(1):45-55 PubMed
Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub. 2012 Sep;156(3):186-99 PubMed
Biofactors. 2009 Sep-Oct;35(5):460-7 PubMed
Biochim Biophys Acta. 2015 Jan;1848(1 Pt B):211-9 PubMed
Reprod Nutr Dev. 2005 Sep-Oct;45(5):559-79 PubMed
Chem Biol Interact. 2006 Oct 27;163(1-2):15-28 PubMed
J Nutr. 2002 May;132(5):1012-7 PubMed
Mol Cancer. 2013 Nov 21;12 (1):145 PubMed
Curr Pharm Biotechnol. 2013;14(3):274-88 PubMed
J Chromatogr B Analyt Technol Biomed Life Sci. 2005 Aug 25;823(1):26-36 PubMed
Neuro Endocrinol Lett. 2009;30 Suppl 1:121-7 PubMed
J Bioenerg Biomembr. 2014 Oct;46(5):447-57 PubMed
FASEB J. 2014 Oct;28(10):4247-64 PubMed
Ann N Y Acad Sci. 2015 Sep;1350:77-81 PubMed
Curr Med Chem. 2007;14(29):3059-69 PubMed
Biochim Biophys Acta. 2014 Sep;1841(9):1308-17 PubMed
Eur J Cancer. 2000 Sep;36(14):1844-52 PubMed
Carcinogenesis. 2005 Jun;26(6):1064-76 PubMed
Mediators Inflamm. 2014;2014:848632 PubMed
FASEB J. 2006 Apr;20(6):770-2 PubMed
Curr Opin Clin Nutr Metab Care. 2012 Mar;15(2):122-6 PubMed
Biochem Biophys Res Commun. 2014 Jul 18;450(1):366-71 PubMed
J Bioenerg Biomembr. 2012 Aug;44(4):439-52 PubMed
Mol Cell. 2012 Nov 30;48(4):612-26 PubMed
Mitochondrion. 2014 May;16:55-64 PubMed
Cancer Res. 2003 Oct 1;63(19):6311-9 PubMed
J Nutr. 2003 Nov;133(11):3509-15 PubMed
Int J Mol Sci. 2012 Nov 21;13(11):15447-63 PubMed
J Nutr. 2002 Dec;132(12):3804S-3808S PubMed
Biochem Cell Biol. 2004 Feb;82(1):18-26 PubMed
Eur J Nutr. 2010 Apr;49(3):133-9 PubMed
J Nutr. 1993 Nov;123(11):1808-17 PubMed
BMC Biochem. 2005 Mar 24;6:5 PubMed
J Nutr. 2004 Dec;134(12 ):3233-8 PubMed
Biophys J. 2015 Sep 15;109(6):1282-94 PubMed
Aliment Pharmacol Ther. 2008 Jan 15;27(2):104-19 PubMed
J Biol Chem. 2006 May 12;281(19):13548-58 PubMed
Chem Phys Lipids. 2008 May;153(1):14-23 PubMed
Proc Natl Acad Sci U S A. 2011 Feb 1;108(5):1903-7 PubMed
Eur J Nutr. 2000 Aug;39(4):164-71 PubMed
Nutr Res Rev. 2004 Dec;17(2):177-92 PubMed
Am J Physiol Gastrointest Liver Physiol. 2002 Aug;283(2):G340-6 PubMed
Biochim Biophys Acta. 1993 Apr 7;1167(2):131-6 PubMed
Biochim Biophys Acta. 2010 Aug;1797(8):1555-62 PubMed
Biochim Biophys Acta. 2009 Oct;1788(10):2022-31 PubMed
Int J Cancer. 2008 Oct 15;123(8):1974-7 PubMed
Am J Physiol Cell Physiol. 2007 Jan;292(1):C33-44 PubMed
Curr Opin Clin Nutr Metab Care. 2007 Jul;10(4):427-32 PubMed
Can J Biochem Physiol. 1959 Aug;37(8):911-7 PubMed
Cancer Metastasis Rev. 2011 Dec;30(3-4):325-42 PubMed
Apoptosis. 2007 May;12(5):877-85 PubMed
Eur J Nutr. 2005 Feb;44(1):40-51 PubMed
FEBS J. 2006 Jun;273(12):2749-65 PubMed
J Lipid Res. 2008 Dec;49(12):2545-56 PubMed
Adv Med Sci. 2007;52:83-8 PubMed
Curr Pharm Des. 2009;15(36):4103-16 PubMed
Cancer Res. 2007 Jun 1;67(11):5561-8 PubMed
Eur J Biochem. 2000 Nov;267(21):6435-42 PubMed
Mol Nutr Food Res. 2008 Aug;52(8):885-97 PubMed
Prog Lipid Res. 2013 Oct;52(4):513-28 PubMed
J Nutr Biochem. 2012 Jun;23(6):539-48 PubMed
J Nutr Biochem. 2004 Nov;15(11):700-6 PubMed
Nat Rev Mol Cell Biol. 2008 Feb;9(2):139-50 PubMed
Mol Nutr Food Res. 2009 May;53 Suppl 1:S102-13 PubMed
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