Ceramide Induces Non-Apoptotic Cell Death in Human Glioma Cells

2005 ◽  
Vol 30 (8) ◽  
pp. 969-979 ◽  
Author(s):  
Wi Hyun Kim ◽  
Chang Hwa Choi ◽  
Soo Kyung Kang ◽  
Chae Hwa Kwon ◽  
Yong Keun Kim
Keyword(s):  
Cell Death ◽  
Apoptotic Cell ◽  
Glioma Cells ◽  
Apoptotic 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 Induction of Lysosomal Membrane Permeabilization Is a Major Event of FTY720-Mediated Non-Apoptotic Cell Death in Human Glioma Cells

Cancers ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3388
Author(s):  
Kyoung-jin Min ◽  
Taeg Kyu Kwon
Keyword(s):  
Cell Death ◽  
Apoptotic Cell ◽  
Ectopic Expression ◽  
Glioma Cells ◽  
Membrane Permeabilization ◽  
Apoptotic Cell Death ◽  
Lysosomal Membrane ◽  
Human Glioma ◽  
Human Glioma Cells ◽  
Lysosomal Membrane Permeabilization

FTY720, a sphingosine-1-phosphate (S1P) receptor modulator, is a synthetic compound produced by the modification of a metabolite from I. sinclairii. Here, we found that FTY720 induced non-apoptotic cell death in human glioma cells (U251MG, U87MG, and U118MG). FTY720 (10 µM) dramatically induced cytoplasmic vacuolation in glioma cells. However, FTY720-mediated vacuolation and cell death are not associated with autophagy. Genetic or pharmacological inhibition of autophagy did not inhibit FTY720-induced cell death. Herein, we detected that FTY720-induced cytoplasmic vacuoles were stained with lysotracker red, and FTY720 induced lysosomal membrane permeabilization (LMP). Interestingly, cathepsin inhibitors (E64D and pepstatin A) and ectopic expression of heat shock protein 70 (HSP70), which is an endogenous inhibitor of LMP, markedly inhibited FTY720-induced cell death. Our results demonstrated that FTY720 induced non-apoptotic cell death via the induction of LMP in human glioma cells.

Massive apoptotic cell death of human glioma cells via a mitochondrial pathway following 5-aminolevulinic acid-mediated photodynamic therapy

2007 ◽  
Vol 83 (3) ◽  
pp. 223-231 ◽  
Author(s):  
Hiroto Inoue ◽  
Yoshinaga Kajimoto ◽  
Masa-Aki Shibata ◽  
Norio Miyoshi ◽  
Naoko Ogawa ◽  
...  
Keyword(s):  
Cell Death ◽  
Photodynamic Therapy ◽  
Aminolevulinic Acid ◽  
Apoptotic Cell ◽  
Glioma Cells ◽  
Mitochondrial Pathway ◽  
Apoptotic Cell Death ◽  
Human Glioma ◽  
Human Glioma Cells

scholarly journals Indirubin exerts anticancer effects on human glioma cells by inducing apoptosis and autophagy

AMB Express ◽  
2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Zhaohui Li ◽  
Han Wang ◽  
Jun Wei ◽  
Liang Han ◽  
Zhigang Guo
Keyword(s):  
Apoptotic Cell ◽  
Treatment Strategies ◽  
Glioma Cells ◽  
Annexin V ◽  
Metastatic Potential ◽  
Human Glioma ◽  
Human Glioma Cells ◽  
Efficient Treatment ◽  
Cell Percentage ◽  
Anticancer Effects

Abstract Glioma causes significant mortality across the world and the most aggressive type of brain cancer. The incidence of glioma is believed to increase in the next few decades and hence more efficient treatment strategies need to be developed for management of glioma. Herein, we examined the anticancer effects of Indirubin against a panel of human glioma cells and attempted to explore the underlying mechanisms. The results of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay showed that Indirubin could inhibit the growth of all the glioma cells but the lowest IC50 of 12.5 µM was observed against the U87 and U118 glioma cells. Additionally, the cytotoxic effects of Indirubin were comparatively negligible against the normal astrocytes with an IC50 of > 100 µM. Investigation of mechanism of action, revealed that Indirubin exerts growth inhibitory effects on the U87 and U118 glioma cells by autophagic and apoptotic cell death. Annexin V/PI staining assay showed that apoptotic cell percentage increased dose dependently. Apoptosis was associated with increase in Bax decrease in Bcl-2 expressions. Additionally, the expression of autophagic proteins such as LC3II, ATG12, ATG15 and Beclin 1 was also increased. Wound heal assay showed that Indirubin caused remarkable decrease in the migration of the U87 and U118 cells indicative of anti-metastatic potential of Indirubin. Taken together, these results suggest that Indirubin exerts potent anticancer effects on glioma cells and may prove essential in the management of glioma.

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
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