Sodium butyrate sensitizes human colon adenocarcinoma COLO 205 cells to both intrinsic and TNF-alpha-dependent extrinsic apoptosis

Apoptosis : an International Journal on Programmed Cell Death
Beata PajakArkadiusz Orzechowski

Abstract

Overexpression of cFLIP protein seems to be critical in the antiapoptotic mechanism of immune escape of human COLO 205 colon adenocarcinoma cells. Actually, cFLIP appears to inhibit the death receptor ligand-mediated cell death. Application of the metabolic inhibitor sodium butyrate (NaBt), short-chain volatile fatty acid, sensitized COLO 205 cells to TNF-alpha-mediated apoptosis. Western-blot analysis revealed that the susceptibility of human COLO 205 cells to apoptogenic stimuli resulted from time-dependent reduction in cFLIP and simultaneous up-regulation of TNF-R1 protein levels. Additionally, the combined TNF-alpha and NaBt treatment caused cleavage of Bid and caspase-9 activation, as well as cytochrome c release from mitochondria. Thus, the evidence of this study indicates that NaBt facilitates the death receptor signal evoked by TNF-alpha. Moreover, NaBt alone initiated intrinsic apoptosis, that in turn was abolished by intracellular BCL-2 delivery. It confirms the involvement of mitochondria in the proapoptotic activity of NaBt. The activation of mitochondrial pathway was substantiated by up-regulated expression of BAK with concomitant reduction of antiapoptotic BCL-x(L), XIAP and survivin proteins. These findings sugge...Continue Reading

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Citations

Jul 28, 2011·Tumour Biology : the Journal of the International Society for Oncodevelopmental Biology and Medicine·Ines Zidi, Nidhal Ben Amor
Jun 9, 2012·The British Journal of Nutrition·Kim Y C FungDavid L Topping
Jan 21, 2010·International Journal of Cancer. Journal International Du Cancer·Katalin DarvasFrank Rösl
Jun 29, 2013·International Journal of Molecular Sciences·Kim Y C FungDavid L Topping

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