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RAD001 (everolimus) enhances TRAIL cytotoxicity in human leukemic Jurkat T cells by upregulating DR5

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), either alone or in combination with other anti-cancer agents, is a promising new strategy for the treatment of cancer. However, aberrant PI3K/Akt/mTOR survival signaling may confer TRAIL resistance by altering the balance between pro-... Full description

Journal Title: Biochemical and Biophysical Research Communications 07 August 2015, Vol.463(4), pp.894-899
Main Author: Lee, Myoung Woo
Other Authors: Kim, Dae Seong , Eom, Ji-Eun , Ko, Young Jong , Sung, Ki Woong , Koo, Hong Hoe , Yoo, Keon Hee
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: ISSN: 0006-291X ; E-ISSN: 1090-2104 ; DOI: 10.1016/j.bbrc.2015.05.133
Link: http://dx.doi.org/10.1016/j.bbrc.2015.05.133
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recordid: elsevier_sdoi_10_1016_j_bbrc_2015_05_133
title: RAD001 (everolimus) enhances TRAIL cytotoxicity in human leukemic Jurkat T cells by upregulating DR5
format: Article
creator:
  • Lee, Myoung Woo
  • Kim, Dae Seong
  • Eom, Ji-Eun
  • Ko, Young Jong
  • Sung, Ki Woong
  • Koo, Hong Hoe
  • Yoo, Keon Hee
subjects:
  • Rad001 (Everolimus)
  • Trail
  • Death Receptor
  • Leukemic Cells
  • Apoptosis
  • Rad001 (Everolimus)
  • Trail
  • Death Receptor
  • Leukemic Cells
  • Apoptosis
  • Biology
  • Chemistry
  • Anatomy & Physiology
ispartof: Biochemical and Biophysical Research Communications, 07 August 2015, Vol.463(4), pp.894-899
description: Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), either alone or in combination with other anti-cancer agents, is a promising new strategy for the treatment of cancer. However, aberrant PI3K/Akt/mTOR survival signaling may confer TRAIL resistance by altering the balance between pro- and anti-apoptotic proteins. In the present study, we showed that the Akt/mTOR inhibitor RAD001 (everolimus) induced cell death in a dose-dependent manner and enhanced TRAIL-induced apoptosis in human leukemic Jurkat T cells, which show PI3K/Akt/mTOR pathway activation and basal expression levels of death receptor (DR) 5 (TRAIL-R2). Investigation of the effect of RAD001 treatment on the expression of TRAIL receptors (TRAIL-Rs) in Jurkat T cells showed that RAD001 significantly upregulated DR5 by up to 51.22%, but not other TRAIL-Rs such as DR4 (TRAIL-R1), decoy receptor (DcR) 1 (TRAIL-R3), and DcR2 (TRAIL-R4). Pretreatment with DR5:Fc chimera abrogated the RAD001-induced increase of...
language: eng
source:
identifier: ISSN: 0006-291X ; E-ISSN: 1090-2104 ; DOI: 10.1016/j.bbrc.2015.05.133
fulltext: fulltext
issn:
  • 0006-291X
  • 0006291X
  • 1090-2104
  • 10902104
url: Link


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titleRAD001 (everolimus) enhances TRAIL cytotoxicity in human leukemic Jurkat T cells by upregulating DR5
creatorLee, Myoung Woo ; Kim, Dae Seong ; Eom, Ji-Eun ; Ko, Young Jong ; Sung, Ki Woong ; Koo, Hong Hoe ; Yoo, Keon Hee
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subjectRad001 (Everolimus) ; Trail ; Death Receptor ; Leukemic Cells ; Apoptosis ; Rad001 (Everolimus) ; Trail ; Death Receptor ; Leukemic Cells ; Apoptosis ; Biology ; Chemistry ; Anatomy & Physiology
descriptionTumor necrosis factor-related apoptosis-inducing ligand (TRAIL), either alone or in combination with other anti-cancer agents, is a promising new strategy for the treatment of cancer. However, aberrant PI3K/Akt/mTOR survival signaling may confer TRAIL resistance by altering the balance between pro- and anti-apoptotic proteins. In the present study, we showed that the Akt/mTOR inhibitor RAD001 (everolimus) induced cell death in a dose-dependent manner and enhanced TRAIL-induced apoptosis in human leukemic Jurkat T cells, which show PI3K/Akt/mTOR pathway activation and basal expression levels of death receptor (DR) 5 (TRAIL-R2). Investigation of the effect of RAD001 treatment on the expression of TRAIL receptors (TRAIL-Rs) in Jurkat T cells showed that RAD001 significantly upregulated DR5 by up to 51.22%, but not other TRAIL-Rs such as DR4 (TRAIL-R1), decoy receptor (DcR) 1 (TRAIL-R3), and DcR2 (TRAIL-R4). Pretreatment with DR5:Fc chimera abrogated the RAD001-induced increase of...
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titleRAD001 (everolimus) enhances TRAIL cytotoxicity in human leukemic Jurkat T cells by upregulating DR5
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Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), either alone or in combination with other anti-cancer agents, is a promising new strategy for the treatment of cancer. However, aberrant PI3K/Akt/mTOR survival signaling may confer TRAIL resistance by altering the balance between pro- and anti-apoptotic proteins. In the present study, we showed that the Akt/mTOR inhibitor RAD001 (everolimus) induced cell death in a dose-dependent manner and enhanced TRAIL-induced apoptosis in human leukemic Jurkat T cells, which show PI3K/Akt/mTOR pathway activation and basal expression levels of death receptor (DR) 5 (TRAIL-R2). Investigation of the effect of RAD001 treatment on the expression of TRAIL receptors (TRAIL-Rs) in Jurkat T cells showed that RAD001 significantly upregulated DR5 by up to 51.22%, but not other TRAIL-Rs such as DR4 (TRAIL-R1), decoy receptor (DcR) 1 (TRAIL-R3), and DcR2 (TRAIL-R4). Pretreatment with DR5:Fc chimera abrogated the RAD001-induced increase of...

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Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), either alone or in combination with other anti-cancer agents, is a promising new strategy for the treatment of cancer. However, aberrant PI3K/Akt/mTOR survival signaling may confer TRAIL resistance by altering the balance between pro- and anti-apoptotic proteins. In the present study, we showed that the Akt/mTOR inhibitor RAD001 (everolimus) induced cell death in a dose-dependent manner and enhanced TRAIL-induced apoptosis in human leukemic Jurkat T cells, which show PI3K/Akt/mTOR pathway activation and basal expression levels of death receptor (DR) 5 (TRAIL-R2). Investigation of the effect of RAD001 treatment on the expression of TRAIL receptors (TRAIL-Rs) in Jurkat T cells showed that RAD001 significantly upregulated DR5 by up to 51.22%, but not other TRAIL-Rs such as DR4 (TRAIL-R1), decoy receptor (DcR) 1 (TRAIL-R3), and DcR2 (TRAIL-R4). Pretreatment with DR5:Fc chimera abrogated the RAD001-induced increase of...

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doi10.1016/j.bbrc.2015.05.133
lad01Biochemical and Biophysical Research Communications
date2015-08-07