About: ROS mediate selenite-induced apoptosis in colon cancer cells

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About: ROS mediate selenite-induced apoptosis in colon cancer cells Goto Sponge NotDistinct Permalink

An Entity of Type : http://linked.opendata.cz/ontology/domain/vavai/Vysledek, within Data Space : linked.opendata.cz associated with source document(s)

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rdf:type	skos:Concept http://linked.opendata.cz/ontology/domain/vavai/Vysledek
Description	Selenite-induced oxidative stress and its relationship to mitochondrial apoptosis was studied in human adenocarcinoma HT-29 cells. It is shown that selenite induces caspase-dependent apoptosis, which is mediated by mitochondria via released cytochrome c, apoptosis-inducing factor (AIF) and Smac/Diablo. Selenite activates stress kinases p38 and JNK while suppressing reduced glutathione (GSH) and thioredoxin reductase (TrxR) levels, transiently inducing heme oxygenase (HO-1) system as well as reducing Akt expression. Pre-treatment of cells with selected antioxidants and stress kinase inhibitors significantly prevented selenite-induced cell death, thereby implicating oxidative stress as a direct (Bax) as well as indirect (via kinases) cause of HT-29 cells demise. These results thus demonstrate for the first time active proapoptotic and anti-survival effects of selenite in colon cancer cells. Selenite-induced oxidative stress and its relationship to mitochondrial apoptosis was studied in human adenocarcinoma HT-29 cells. It is shown that selenite induces caspase-dependent apoptosis, which is mediated by mitochondria via released cytochrome c, apoptosis-inducing factor (AIF) and Smac/Diablo. Selenite activates stress kinases p38 and JNK while suppressing reduced glutathione (GSH) and thioredoxin reductase (TrxR) levels, transiently inducing heme oxygenase (HO-1) system as well as reducing Akt expression. Pre-treatment of cells with selected antioxidants and stress kinase inhibitors significantly prevented selenite-induced cell death, thereby implicating oxidative stress as a direct (Bax) as well as indirect (via kinases) cause of HT-29 cells demise. These results thus demonstrate for the first time active proapoptotic and anti-survival effects of selenite in colon cancer cells. (en)
Title	ROS mediate selenite-induced apoptosis in colon cancer cells ROS mediate selenite-induced apoptosis in colon cancer cells (en)
skos:prefLabel	ROS mediate selenite-induced apoptosis in colon cancer cells ROS mediate selenite-induced apoptosis in colon cancer cells (en)
skos:notation	RIV/00216208:11150/10:10072265!RIV11-MSM-11150___
http://linked.open...avai/riv/aktivita	Z
http://linked.open...avai/riv/aktivity	Z(MSM0021620820)
http://linked.open...iv/cisloPeriodika	2
http://linked.open...vai/riv/dodaniDat	2011
http://linked.open...aciTvurceVysledku	Červinka, Miroslav Rudolf, Emil Králová, Věra
http://linked.open.../riv/druhVysledku	J - Článek v odborném periodiku
http://linked.open...iv/duvernostUdaju	S - Úplné a pravdivé údaje nepodléhající ochraně podle zvláštních právních předpisů
http://linked.open...titaPredkladatele	Univerzita Karlova v Praze / Lékařská fakulta v Hradci Králové
http://linked.open...dnocenehoVysledku	285847
http://linked.open...ai/riv/idVysledku	RIV/00216208:11150/10:10072265
http://linked.open...riv/jazykVysledku	eng - angličtina
http://linked.open.../riv/klicovaSlova	HO-1; Smac/Diablo; ROS; kinases; colon cancer; mitochondria; Selenite (en)
http://linked.open.../riv/klicoveSlovo	Selenite ROS HO-1 mitochondria kinases colon cancer Smac/Diablo
http://linked.open...odStatuVydavatele	PL - Polská republika
http://linked.open...ontrolniKodProRIV	[C82A305A390F]
http://linked.open...i/riv/nazevZdroje	Central European Journal of Biology
http://linked.open...in/vavai/riv/obor	EB
http://linked.open...ichTvurcuVysledku	3 (xsd:int)
http://linked.open...cetTvurcuVysledku	3 (xsd:int)
http://linked.open...UplatneniVysledku	2010
http://linked.open...v/svazekPeriodika	5
http://linked.open...iv/tvurceVysledku	Rudolf, Emil Červinka, Miroslav Králová, Věra
http://linked.open...ain/vavai/riv/wos	000275141000004
http://linked.open...n/vavai/riv/zamer	The use of experimental and clinical models of metabolic processes, nutrition and pharmacotherapy for the advancement of knowledge, clinical practice and quality of life improvement
issn	1895-104X
number of pages	12 (xsd:int)
http://localhost/t...ganizacniJednotka	11150

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