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dc.contributor.authorSohn, Vanessa R.
dc.contributor.authorGiros, Anna
dc.contributor.authorXicola, Rosa M.
dc.contributor.authorGrzybowski, Mike
dc.contributor.authorAnguera, Anna
dc.contributor.authorLlor, Xavier
dc.contributor.author Fluvià, Lourdes
dc.date.accessioned2013-11-01T15:31:14Z
dc.date.available2013-12-06T23:26:12Z
dc.date.issued2012-06
dc.identifier.bibliographicCitationSohn VR, Giros A, Xicola RM, Fluvià L, Grzybowski M, Anguera A, Llor X. Stool-fermented Plantago ovata husk induces apoptosis in colorectal cancer cells independently of molecular phenotype. Br J Nutr. 2012 Jun;107(11):1591-602. DOI; 10.1017/S0007114511004910en_US
dc.identifier.issn1475-2662
dc.identifier.urihttp://hdl.handle.net/10027/10388
dc.descriptionThis is a copy of an article published in the British Journal of Nutrition. © 2012 Cambridge University Press.en_US
dc.description.abstractSeveral studies have suggested that the partially fermentable fibre Plantago ovata husk (PO) may have a protective effect on colorectal cancer (CRC). We studied the potentially pro-apoptotic effect of PO and the implicated mechanisms in CRC cells with different molecular phenotypes (Caco-2, HCT116, LoVo, HT-29, SW480) after PO anaerobic fermentation with colonic bacteria as it occurs in the human colon. The fermentation products of PO induced apoptosis in all primary tumour and metastatic cell lines, independent of p53, adenomatous polyposis coli, b-catenin or cyclo-oxygenase-2 status. Apoptosis was caspase-dependent and both intrinsic and extrinsic pathways were implicated. The intrinsic pathway was activated through a shift in the balance towards a pro-apoptotic environment with an up-regulation of B-cell lymphoma protein 2 homologous antagonist killer (BAK) and a down-regulation of B-cell lymphoma-extra large (Bcl-xL) seen in HCT116 and LoVo cells. This resulted in mitochondrial membrane depolarisation, increased expression of caspase activators second mitochondria- derived activator of caspases (Smac)/Diablo, death effector apoptosis-inducing factor, apoptosome member apoptotic protease activating factor 1 and down-regulation of inhibitors of apoptosis Survivin and X-linked inhibitor of apoptosis in most cells. The extrinsic pathway was activated presumably through the up-regulation of death receptor (DR5). Some important differences were seen between primary tumour and metastatic CRC cells. Thus, metastatic PO-treated LoVo cells had a remarkable up-regulation of TNF-a ligand along with death-inducing signalling complex components receptor interacting protein and TNF-a receptor 1-associated death domain protein. The extrinsic pathway modulator FCICE-inhibitory protein (FLIP), an inhibitor of both spontaneous death ligand-independent and death receptor-mediated apoptosis, was significantly down-regulated after PO treatment in all primary tumour cells, but not in metastatic LoVo. These findings suggest that PO could potentially be a useful chemotherapy adjuvant.en_US
dc.description.sponsorshipThe present research was supported by grant no. 2007-01934 from Rottapharm S. L. and Departmental grants from the University of Illinois at Chicago Department of Medicine and Cancer Centeren_US
dc.language.isoen_USen_US
dc.publisherCambridge University Pressen_US
dc.subjectColon canceren_US
dc.subjectApoptosisen_US
dc.subjectPlantago ovata husken_US
dc.titleStool-fermented Plantago ovata husk induces apoptosis in colorectal cancer cells independently of molecular phenotypeen_US
dc.typeArticleen_US


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