15-Deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2) Induces Cell Death Through Caspase-independent Mechanism in A172 Human Glioma Cells

2006 ◽  
Vol 31 (10) ◽  
pp. 1247-1254 ◽  
Author(s):  
W. H. Cho ◽  
C. H. Choi ◽  
J. Y. Park ◽  
S. K. Kang ◽  
Y. K. Kim
Keyword(s):  
Cell Death ◽  
Glioma Cells ◽  
Human Glioma ◽  
Human Glioma Cells ◽  
Independent Mechanism ◽  
Prostaglandin J2

scholarly journals Diva/Boo is a negative regulator of cell death in human glioma cells

FEBS Letters ◽  
2001 ◽  
Vol 505 (1) ◽  
pp. 23-26 ◽  
Author(s):  
Ulrike Naumann ◽  
Simone Weit ◽  
Jörg Wischhusen ◽  
Michael Weller
Keyword(s):  
Cell Death ◽  
Glioma Cells ◽  
Negative Regulator ◽  
Human Glioma ◽  
Human Glioma Cells

Synergistic cytotoxicity through the activation of multiple apoptosis pathways in human glioma cells induced by combined treatment with ionizing radiation and tumor necrosis factor–related apoptosis-inducing ligand

2007 ◽  
Vol 106 (3) ◽  
pp. 407-416 ◽  
Author(s):  
Motoo Nagane ◽  
Webster K. Cavenee ◽  
Yoshiaki Shiokawa
Keyword(s):  
Cell Death ◽  
Ionizing Radiation ◽  
Combination Treatment ◽  
Tumor Necrosis ◽  
Malignant Gliomas ◽  
Glioma Cells ◽  
Caspase 8 ◽  
Human Glioma ◽  
Human Glioma Cells ◽  
Necrosis Factor

Object Malignant gliomas remain incurable despite modern multimodality treatments. Tumor necrosis factor (TNF)–related apoptosis-inducing ligand (TRAIL), also known as Apo2L, a member of the TNF family, preferentially induces apoptosis in human tumor cells through its cognate death receptors DR4 or DR5, suggesting that it may serve as a potential therapeutic agent for intractable malignant gliomas. Here, the authors show that genotoxic ionizing radiation synergistically enhances TRAIL-induced cell death in human glioma cells expressing DR5. Methods Combination treatment with soluble human TRAIL plus radiation induced robust cell death, while each of them singly led to only limited cytotoxicity. The combination resulted in cleavage and activation of the apoptotic initiator caspase-8 and the effector caspase-3 as well as cleavage of Bid and another initiator caspase-9, a downstream component of the apoptosome. Accordingly, it augmented the release of cytochrome c from the mitochondria into the cytosol, as well as apoptosis-inducing factor. Synergistic cell death was suppressed by TRAIL-neutralizing DR5-Fc, caspase inhibitors, expression of dominant-negative Fasassociated protein with death domain and CrmA, which selectively blocks caspase-8, and overexpression of Bcl-XL. Finally, combination treatment had no influence on the viability of normal human astrocytes. Conclusions These results suggest that combination treatment with TRAIL and ionizing radiation kills human glioma cells through the activation of DR5-mediated death receptor pathways. This therapy involves direct activation of effector caspases as well as mitochondria-mediated pathways and provides a novel strategy in which TRAIL could be synergistically combined with DNA-damaging radiation.

Role of ERK in Hydrogen Peroxide-Induced Cell Death of Human Glioma Cells

2005 ◽  
Vol 30 (2) ◽  
pp. 263-270 ◽  
Author(s):  
Won Chang Lee ◽  
Chang Hwa Choi ◽  
Seung Heon Cha ◽  
Hyun Lim Oh ◽  
Yong Keun Kim
Keyword(s):  
Hydrogen Peroxide ◽  
Cell Death ◽  
Glioma Cells ◽  
Human Glioma ◽  
Human Glioma Cells

Protection Against Arsenic Trioxide-Induced Autophagic Cell Death in U118 Human Glioma Cells by Use of Lipoic Acid

Epidemiology ◽  
2006 ◽  
Vol 17 (Suppl) ◽  
pp. S495-S496
Author(s):  
Y J Wang ◽  
T J Cheng ◽  
W W Kao ◽  
R J Chen ◽  
Y S Ho
Keyword(s):  
Cell Death ◽  
Arsenic Trioxide ◽  
Lipoic Acid ◽  
Glioma Cells ◽  
Autophagic Cell Death ◽  
Human Glioma ◽  
Human Glioma Cells

Video-enhanced microscopic visualization of apoptotic cell death caused by anti-Fas antibody in living human glioma cells

1998 ◽  
Vol 15 (1) ◽  
pp. 19-21
Author(s):  
Seiji Ohta ◽  
Jun Yoshida ◽  
Seiji Yamamoto ◽  
Kenichi Uemura ◽  
Toshihiko Wakabayashi ◽  
...  
Keyword(s):  
Cell Death ◽  
Apoptotic Cell ◽  
Glioma Cells ◽  
Apoptotic Cell Death ◽  
Human Glioma ◽  
Human Glioma Cells

scholarly journals P04.50 Doxycycline impairs mitochondrial function and protects human glioma cells from hypoxia-induced cell death: implications of using Tet-inducible systems

2018 ◽  
Vol 20 (suppl_3) ◽  
pp. iii290-iii290
Author(s):  
B Sauer ◽  
A Luger ◽  
N I Lorenz ◽  
A L Engel ◽  
Y Braun ◽  
...  
Keyword(s):  
Cell Death ◽  
Mitochondrial Function ◽  
Glioma Cells ◽  
Human Glioma ◽  
Human Glioma Cells ◽  
Inducible Systems

Temozolomide and sorafenib as programmed cell death inducers of human glioma cells

2017 ◽  
Vol 69 (4) ◽  
pp. 779-787 ◽  
Author(s):  
Joanna Jakubowicz-Gil ◽  
Dorota Bądziul ◽  
Ewa Langner ◽  
Iwona Wertel ◽  
Adrian Zając ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Glioma Cells ◽  
Human Glioma ◽  
Human Glioma Cells

scholarly journals Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand Induces Caspase-Dependent Interleukin-8 Expression and Apoptosis in Human Astroglioma Cells

2002 ◽  
Vol 22 (3) ◽  
pp. 724-736 ◽  
Author(s):  
Chulhee Choi ◽  
Olaf Kutsch ◽  
Jinseu Park ◽  
Tong Zhou ◽  
Dai-Wu Seol ◽  
...  
Keyword(s):  
Cell Death ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Glioma Cells ◽  
Interleukin 8 ◽  
Human Glioma ◽  
Caspase Activation ◽  
Human Glioma Cells ◽  
Necrosis Factor ◽  
Specific Inhibitors

ABSTRACT Among the tumor necrosis factor (TNF) family of cytokines, FasL and TNF-related apoptosis-inducing ligand (TRAIL) are known to induce cell death via caspase activation. Recently, other biological functions of these death ligands have been postulated in vitro and in vivo. It was previously shown that Fas ligation induces chemokine expression in human glioma cells. In this study, we investigated whether the TRAIL-DR5 system transduces signals similar to those induced by other TNF family ligands and receptors. To address this issue, two human glioma cell lines, CRT-MG and U87-MG, were used, and an agonistic antibody against DR5 (TRA-8) and human recombinant TRAIL were used to ligate DR5. We demonstrate that DR5 ligation by either TRAIL or TRA-8 induces two functional outcomes, apoptosis and expression of the chemokine interleukin-8 (IL-8); the nonspecific caspase inhibitor Boc-D-Fmk blocks both TRAIL-mediated cell death and IL-8 production; the caspase 3-specific inhibitor z-DEVD-Fmk suppresses TRAIL-mediated apoptosis but not IL-8 induction; caspase 1- and 8-specific inhibitors block both TRAIL-mediated cell death and IL-8 production; and DR5 ligation by TRAIL mediates AP-1 and NF-κB activation, which can be inhibited by caspase 1- and 8-specific inhibitors. These findings collectively indicate that DR5 ligation on human glioma cells leads to apoptosis and that the activation of AP-1 and NF-κB leads to the induction of IL-8 expression; these responses are dependent on caspase activation. Therefore, the TRAIL-DR5 system has a role not only as an inducer of apoptotic cell death but also as a tranducer for proinflammatory and angiogenic signals in human brain tumors.

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