Cell death is induced by ciglitazone, a peroxisome proliferator-activated receptor {gamma} (PPAR{gamma}) agonist, independently of PPAR{gamma} in human glioma cells
Abstract
Highlights: Black-Right-Pointing-Pointer Greater than 30 {mu}M ciglitazone induces cell death in glioma cells. Black-Right-Pointing-Pointer Cell death by ciglitazone is independent of PPAR{gamma} in glioma cells. Black-Right-Pointing-Pointer CGZ induces cell death by the loss of MMP via decreased Akt. -- Abstract: Peroxisome proliferator-activated receptor {gamma} (PPAR{gamma}) 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 PPAR{gamma} in CGZ-induced cell death was examined. At concentrations of greater than 30 {mu}M, CGZ, a synthetic PPAR{gamma} agonist, activated caspase-3 and induced apoptosis in T98G cells. Treatment of T98G cells with less than 30 {mu}M CGZ effectively induced cell death after pretreatment with 30 {mu}M of the PPAR{gamma} 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. In cells in which PPAR{gamma} was down-regulated cells by siRNA, lower concentrations of CGZ (<30 {mu}M) were sufficient to induce cell death, although higher concentrations of CGZ ( Greater-Than-Or-Slanted-Equal-To 30 {mu}M) were required to induce cell death in controlmore »
- Authors:
-
- Department of Pediatrics, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul (Korea, Republic of)
- Publication Date:
- OSTI Identifier:
- 22207640
- Resource Type:
- Journal Article
- Journal Name:
- Biochemical and Biophysical Research Communications
- Additional Journal Information:
- Journal Volume: 417; Journal Issue: 1; Other Information: Copyright (c) 2011 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
- Subject:
- 60 APPLIED LIFE SCIENCES; APOPTOSIS; CELL MEMBRANES; GENE REGULATION; GLIOMAS; MITOCHONDRIA; RECEPTORS
Citation Formats
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, E-mail: hhkoo@skku.edu, and Sung, Ki Woong, E-mail: kwsped@skku.edu. Cell death is induced by ciglitazone, a peroxisome proliferator-activated receptor {gamma} (PPAR{gamma}) agonist, independently of PPAR{gamma} in human glioma cells. United States: N. p., 2012.
Web. doi:10.1016/J.BBRC.2011.12.001.
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, E-mail: hhkoo@skku.edu, & Sung, Ki Woong, E-mail: kwsped@skku.edu. Cell death is induced by ciglitazone, a peroxisome proliferator-activated receptor {gamma} (PPAR{gamma}) agonist, independently of PPAR{gamma} in human glioma cells. United States. https://doi.org/10.1016/J.BBRC.2011.12.001
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, E-mail: hhkoo@skku.edu, and Sung, Ki Woong, E-mail: kwsped@skku.edu. 2012.
"Cell death is induced by ciglitazone, a peroxisome proliferator-activated receptor {gamma} (PPAR{gamma}) agonist, independently of PPAR{gamma} in human glioma cells". United States. https://doi.org/10.1016/J.BBRC.2011.12.001.
@article{osti_22207640,
title = {Cell death is induced by ciglitazone, a peroxisome proliferator-activated receptor {gamma} (PPAR{gamma}) agonist, independently of PPAR{gamma} in human glioma cells},
author = {Lee, Myoung Woo and Kim, Dae Seong and Kim, Hye Ryung and Kim, Hye Jin and Yang, Jin Mo and Ryu, Somi and Noh, Yoo Hun and Lee, Soo Hyun and Son, Meong Hi and Jung, Hye Lim and Yoo, Keon Hee and Koo, Hong Hoe, E-mail: hhkoo@skku.edu and Sung, Ki Woong, E-mail: kwsped@skku.edu},
abstractNote = {Highlights: Black-Right-Pointing-Pointer Greater than 30 {mu}M ciglitazone induces cell death in glioma cells. Black-Right-Pointing-Pointer Cell death by ciglitazone is independent of PPAR{gamma} in glioma cells. Black-Right-Pointing-Pointer CGZ induces cell death by the loss of MMP via decreased Akt. -- Abstract: Peroxisome proliferator-activated receptor {gamma} (PPAR{gamma}) 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 PPAR{gamma} in CGZ-induced cell death was examined. At concentrations of greater than 30 {mu}M, CGZ, a synthetic PPAR{gamma} agonist, activated caspase-3 and induced apoptosis in T98G cells. Treatment of T98G cells with less than 30 {mu}M CGZ effectively induced cell death after pretreatment with 30 {mu}M of the PPAR{gamma} 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. In cells in which PPAR{gamma} was down-regulated cells by siRNA, lower concentrations of CGZ (<30 {mu}M) were sufficient to induce cell death, although higher concentrations of CGZ ( Greater-Than-Or-Slanted-Equal-To 30 {mu}M) were required to induce cell death in control T98G cells, indicating that CGZ effectively induces cell death in T98G cells independently of PPAR{gamma}. Treatment with GW9662 followed by CGZ resulted in a down-regulation of Akt activity and the loss of mitochondrial membrane potential (MMP), which was accompanied by a decrease in Bcl-2 expression and an increase in Bid cleavage. These data suggest that CGZ is capable of inducing apoptotic cell death independently of PPAR{gamma} in glioma cells, by down-regulating Akt activity and inducing MMP collapse.},
doi = {10.1016/J.BBRC.2011.12.001},
url = {https://www.osti.gov/biblio/22207640},
journal = {Biochemical and Biophysical Research Communications},
issn = {0006-291X},
number = 1,
volume = 417,
place = {United States},
year = {Fri Jan 06 00:00:00 EST 2012},
month = {Fri Jan 06 00:00:00 EST 2012}
}