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Cell death is induced by ciglitazone, a peroxisome proliferator-activated receptor γ (PPARγ) agonist, independently of PPARγ in human glioma cells

► Greater than 30μM ciglitazone induces cell death in glioma cells. ► Cell death by ciglitazone is independent of PPARγ in glioma cells. ► CGZ induces cell death by the loss of MMP via decreased Akt. Peroxisome proliferator-activated receptor γ (PPARγ) regulates multiple signaling pathways, and its... Full description

Journal Title: Biochemical and Biophysical Research Communications 06 January 2012, Vol.417(1), pp.552-557
Main Author: Lee, Myoung Woo
Other Authors: Kim, Dae Seong , Kim, Hye Ryung , Kim, Hye Jin , Yang, Jin Mo , Ryu, Somi , Noh, Yoo Hun , Lee, Soo Hyun , Son, Meong Hi , Jung, Hye Lim , Yoo, Keon Hee , Koo, Hong Hoe , Sung, Ki Woong
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: ISSN: 0006-291X ; E-ISSN: 1090-2104 ; DOI: 10.1016/j.bbrc.2011.12.001
Link: http://dx.doi.org/10.1016/j.bbrc.2011.12.001
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recordid: elsevier_sdoi_10_1016_j_bbrc_2011_12_001
title: Cell death is induced by ciglitazone, a peroxisome proliferator-activated receptor γ (PPARγ) agonist, independently of PPARγ in human glioma cells
format: Article
creator:
  • Lee, Myoung Woo
  • Kim, Dae Seong
  • Kim, Hye Ryung
  • Kim, Hye Jin
  • Yang, Jin Mo
  • Ryu, Somi
  • Noh, Yoo Hun
  • Lee, Soo Hyun
  • Son, Meong Hi
  • Jung, Hye Lim
  • Yoo, Keon Hee
  • Koo, Hong Hoe
  • Sung, Ki Woong
subjects:
  • Pparγ
  • Ciglitazone
  • Gw9662
  • Glioma
  • Apoptosis
  • Pparγ
  • Ciglitazone
  • Gw9662
  • Glioma
  • Apoptosis
  • Biology
  • Chemistry
  • Anatomy & Physiology
ispartof: Biochemical and Biophysical Research Communications, 06 January 2012, Vol.417(1), pp.552-557
description: ► Greater than 30μM ciglitazone induces cell death in glioma cells. ► Cell death by ciglitazone is independent of PPARγ in glioma cells. ► CGZ induces cell death by the loss of MMP via decreased Akt. Peroxisome proliferator-activated receptor γ (PPARγ) regulates multiple signaling pathways, and its agonists induce apoptosis in various cancer cells. However, their role in cell death is unclear. In this study, the relationship between ciglitazone (CGZ) and PPARγ in CGZ-induced cell death was examined. At concentrations of greater than 30μM, CGZ, a synthetic PPARγ agonist, activated caspase-3 and induced apoptosis in T98G cells. Treatment of T98G cells with less than 30μM CGZ effectively induced cell death after pretreatment with 30μM of the PPARγ antagonist GW9662, although GW9662 alone did not induce cell death. This cell death was also observed when cells were co-treated with CGZ and GW9662, but was not observed when cells were treated with CGZ prior to GW9662....
language: eng
source:
identifier: ISSN: 0006-291X ; E-ISSN: 1090-2104 ; DOI: 10.1016/j.bbrc.2011.12.001
fulltext: fulltext
issn:
  • 0006-291X
  • 0006291X
  • 1090-2104
  • 10902104
url: Link


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titleCell death is induced by ciglitazone, a peroxisome proliferator-activated receptor γ (PPARγ) agonist, independently of PPARγ in human glioma cells
creatorLee, Myoung Woo ; Kim, Dae Seong ; Kim, Hye Ryung ; Kim, Hye Jin ; Yang, Jin Mo ; Ryu, Somi ; Noh, Yoo Hun ; Lee, Soo Hyun ; Son, Meong Hi ; Jung, Hye Lim ; Yoo, Keon Hee ; Koo, Hong Hoe ; Sung, Ki Woong
ispartofBiochemical and Biophysical Research Communications, 06 January 2012, Vol.417(1), pp.552-557
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subjectPparγ ; Ciglitazone ; Gw9662 ; Glioma ; Apoptosis ; Pparγ ; Ciglitazone ; Gw9662 ; Glioma ; Apoptosis ; Biology ; Chemistry ; Anatomy & Physiology
description► Greater than 30μM ciglitazone induces cell death in glioma cells. ► Cell death by ciglitazone is independent of PPARγ in glioma cells. ► CGZ induces cell death by the loss of MMP via decreased Akt. Peroxisome proliferator-activated receptor γ (PPARγ) regulates multiple signaling pathways, and its agonists induce apoptosis in various cancer cells. However, their role in cell death is unclear. In this study, the relationship between ciglitazone (CGZ) and PPARγ in CGZ-induced cell death was examined. At concentrations of greater than 30μM, CGZ, a synthetic PPARγ agonist, activated caspase-3 and induced apoptosis in T98G cells. Treatment of T98G cells with less than 30μM CGZ effectively induced cell death after pretreatment with 30μM of the PPARγ antagonist GW9662, although GW9662 alone did not induce cell death. This cell death was also observed when cells were co-treated with CGZ and GW9662, but was not observed when cells were treated with CGZ prior to GW9662....
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titleCell death is induced by ciglitazone, a peroxisome proliferator-activated receptor γ (PPARγ) agonist, independently of PPARγ in human glioma cells
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► Greater than 30μM ciglitazone induces cell death in glioma cells. ► Cell death by ciglitazone is independent of PPARγ in glioma cells. ► CGZ induces cell death by the loss of MMP via decreased Akt.

Peroxisome proliferator-activated receptor γ (PPARγ) regulates multiple signaling pathways, and its agonists induce apoptosis in various cancer cells. However, their role in cell death is unclear. In this study, the relationship between ciglitazone (CGZ) and PPARγ in CGZ-induced cell death was examined. At concentrations of greater than 30μM, CGZ, a synthetic PPARγ agonist, activated caspase-3 and induced apoptosis in T98G cells. Treatment of T98G cells with less than 30μM CGZ effectively induced cell death after pretreatment with 30μM of the PPARγ antagonist GW9662, although GW9662 alone did not induce cell death. This cell death was also observed when cells were co-treated with CGZ and GW9662, but was not observed when cells were treated with CGZ prior to GW9662....

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authorLee, Myoung Woo ; Kim, Dae Seong ; Kim, Hye Ryung ; Kim, Hye Jin ; Yang, Jin Mo ; Ryu, Somi ; Noh, Yoo Hun ; Lee, Soo Hyun ; Son, Meong Hi ; Jung, Hye Lim ; Yoo, Keon Hee ; Koo, Hong Hoe ; Sung, Ki Woong
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► Greater than 30μM ciglitazone induces cell death in glioma cells. ► Cell death by ciglitazone is independent of PPARγ in glioma cells. ► CGZ induces cell death by the loss of MMP via decreased Akt.

Peroxisome proliferator-activated receptor γ (PPARγ) regulates multiple signaling pathways, and its agonists induce apoptosis in various cancer cells. However, their role in cell death is unclear. In this study, the relationship between ciglitazone (CGZ) and PPARγ in CGZ-induced cell death was examined. At concentrations of greater than 30μM, CGZ, a synthetic PPARγ agonist, activated caspase-3 and induced apoptosis in T98G cells. Treatment of T98G cells with less than 30μM CGZ effectively induced cell death after pretreatment with 30μM of the PPARγ antagonist GW9662, although GW9662 alone did not induce cell death. This cell death was also observed when cells were co-treated with CGZ and GW9662, but was not observed when cells were treated with CGZ prior to GW9662....

pubElsevier Inc
doi10.1016/j.bbrc.2011.12.001
lad01Biochemical and Biophysical Research Communications
date2012-01-06