About: Transformation by oncogenic RAS sensitizes human colon cells to TRAIL-induced apoptosis by up-regulating death receptor 4 and death receptor 5 through a MEK-dependent pathway     Goto   Sponge   NotDistinct   Permalink

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  • We show that tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) induces cell death in human colon adenocarcinoma cells in a MEK-dependent manner. We also report a prolonged MEK-dependent activation of ERK1/2 and increased c-FOS expression induced by TRAIL in this system. We reveal that transformation of colon cell line Caco-2 by Ki- and mainly Ha-ras oncogenes sensitizes these cells to TRAIL-induced apoptosis by causing specific MEK-dependent up-regulation of DR4 and DR5. These observations taken together reveal that RAS-MEK-ERK1/2 signaling pathway can sensitize cells to TRAIL-induced apoptosis by up-regulating DR4 and DR5 and overall imply that TRAIL-based therapeutic strategies using TRAIL agonists could be used in cases of human colon cancers bearing RAS mutations.
  • We show that tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) induces cell death in human colon adenocarcinoma cells in a MEK-dependent manner. We also report a prolonged MEK-dependent activation of ERK1/2 and increased c-FOS expression induced by TRAIL in this system. We reveal that transformation of colon cell line Caco-2 by Ki- and mainly Ha-ras oncogenes sensitizes these cells to TRAIL-induced apoptosis by causing specific MEK-dependent up-regulation of DR4 and DR5. These observations taken together reveal that RAS-MEK-ERK1/2 signaling pathway can sensitize cells to TRAIL-induced apoptosis by up-regulating DR4 and DR5 and overall imply that TRAIL-based therapeutic strategies using TRAIL agonists could be used in cases of human colon cancers bearing RAS mutations. (en)
  • Ukazujeme, že TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) vyvolává buněčnou smrt u buněk adenokarcinomu lidského kolonu cestou závislou na MEK. Ukazujeme dále dlouhodobou aktivaci ERK1/2 a zvýšenou expresi c-FOS vyvolanou v tomto systému pomocí TRAIL. Odhalujeme, že transformace buněčné linie kolonu Caco-2 onkogeny Ki- a zejména Ha-ras způsobuje citlivost těchto buněk vůči apoptóze vyvolané TRAIL specifickým zvýšením exprese DR4 a DR5 závislým na MEK. Z těchto pozorování vyplývá, že signální dráha RAS-MEK-ERK1/2 může způsobit citlivost buněk vůči apoptóze vyvolané TRAIL zvýšením exprese DR4 a DR5, a lze tedy souhrnně říci, že léčebné strategie založené na TRAIL a využívající agonisty TRAIL by mohly být využity pro případy nádorů lidského kolonu vyvolané mutacemi RAS. (cs)
Title
  • Transformation by oncogenic RAS sensitizes human colon cells to TRAIL-induced apoptosis by up-regulating death receptor 4 and death receptor 5 through a MEK-dependent pathway
  • Transformation by oncogenic RAS sensitizes human colon cells to TRAIL-induced apoptosis by up-regulating death receptor 4 and death receptor 5 through a MEK-dependent pathway (en)
  • Transformace onkogenním RAS způsobuje citlivost buněk lidského kolonu vůči apoptóze vyvolané TRAIL zvýšením exprese receptoru smrti 4 a receptoru smrti 5 cestou závislou na MEK (cs)
skos:prefLabel
  • Transformation by oncogenic RAS sensitizes human colon cells to TRAIL-induced apoptosis by up-regulating death receptor 4 and death receptor 5 through a MEK-dependent pathway
  • Transformation by oncogenic RAS sensitizes human colon cells to TRAIL-induced apoptosis by up-regulating death receptor 4 and death receptor 5 through a MEK-dependent pathway (en)
  • Transformace onkogenním RAS způsobuje citlivost buněk lidského kolonu vůči apoptóze vyvolané TRAIL zvýšením exprese receptoru smrti 4 a receptoru smrti 5 cestou závislou na MEK (cs)
skos:notation
  • RIV/68378050:_____/05:00001247!RIV06-AV0-68378050
http://linked.open.../vavai/riv/strany
  • 22856;22867
http://linked.open...avai/riv/aktivita
http://linked.open...avai/riv/aktivity
  • P(KJB5052407), P(KSK5020115)
http://linked.open...iv/cisloPeriodika
  • 24
http://linked.open...vai/riv/dodaniDat
http://linked.open...aciTvurceVysledku
http://linked.open.../riv/druhVysledku
http://linked.open...iv/duvernostUdaju
http://linked.open...titaPredkladatele
http://linked.open...dnocenehoVysledku
  • 547071
http://linked.open...ai/riv/idVysledku
  • RIV/68378050:_____/05:00001247
http://linked.open...riv/jazykVysledku
http://linked.open.../riv/klicovaSlova
  • TRAIL; Ras; apoptosis (en)
http://linked.open.../riv/klicoveSlovo
http://linked.open...odStatuVydavatele
  • US - Spojené státy americké
http://linked.open...ontrolniKodProRIV
  • [0E0D6951282B]
http://linked.open...i/riv/nazevZdroje
  • Journal of Biological Chemistry
http://linked.open...in/vavai/riv/obor
http://linked.open...ichTvurcuVysledku
http://linked.open...cetTvurcuVysledku
http://linked.open...vavai/riv/projekt
http://linked.open...UplatneniVysledku
http://linked.open...v/svazekPeriodika
  • 280
http://linked.open...iv/tvurceVysledku
  • Anděra, Ladislav
  • Pintzas, A.
  • Sasazuki, T.
  • Shirasawa, S.
  • Čermák, Lukáš
  • Drosopoulos, K. G.
  • Roberts, M. L.
issn
  • 0021-9258
number of pages
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