Interaction of polyunsaturated fatty acids and sodium butyrate during apoptosis in HT-29 human colon adenocarcinoma cells
Jazyk angličtina Země Německo Médium print-electronic
Typ dokumentu srovnávací studie, časopisecké články, práce podpořená grantem
- MeSH
- adenokarcinom metabolismus MeSH
- apoptóza * účinky léků MeSH
- buněčný cyklus účinky léků MeSH
- buňky HT-29 MeSH
- butyráty metabolismus MeSH
- fluorescenční mikroskopie MeSH
- kaspasa 3 MeSH
- kaspasa 9 MeSH
- kaspasy účinky léků metabolismus MeSH
- kyselina arachidonová aplikace a dávkování MeSH
- kyseliny dokosahexaenové aplikace a dávkování MeSH
- lidé MeSH
- membránové potenciály účinky léků MeSH
- nádory tračníku metabolismus MeSH
- nenasycené mastné kyseliny metabolismus MeSH
- peroxidace lipidů účinky léků MeSH
- poly(ADP-ribosa)-polymerasy účinky léků metabolismus MeSH
- protoonkogenní proteiny účinky léků metabolismus MeSH
- průtoková cytometrie MeSH
- reaktivní formy kyslíku metabolismus MeSH
- vztah mezi dávkou a účinkem léčiva MeSH
- western blotting MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- srovnávací studie MeSH
- Názvy látek
- butyráty MeSH
- CASP3 protein, human MeSH Prohlížeč
- CASP9 protein, human MeSH Prohlížeč
- kaspasa 3 MeSH
- kaspasa 9 MeSH
- kaspasy MeSH
- kyselina arachidonová MeSH
- kyseliny dokosahexaenové MeSH
- nenasycené mastné kyseliny MeSH
- poly(ADP-ribosa)-polymerasy MeSH
- protoonkogenní proteiny MeSH
- reaktivní formy kyslíku MeSH
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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