scholarly journals Identification of RIP1 as a critical mediator of Smac mimetic-mediated sensitization of glioblastoma cells for Drozitumab-induced apoptosis

2015 ◽  
Vol 6 (4) ◽  
pp. e1724-e1724 ◽  
Author(s):  
S Cristofanon ◽  
B A Abhari ◽  
M Krueger ◽  
A Tchoghandjian ◽  
S Momma ◽  
...  
Keyword(s):  
Glioblastoma Cells ◽  
Smac Mimetic ◽  
Induced Apoptosis

scholarly journals Smac mimetic sensitizes glioblastoma cells to Temozolomide-induced apoptosis in a RIP1- and NF-κB-dependent manner

Oncogene ◽  
2012 ◽  
Vol 32 (8) ◽  
pp. 988-997 ◽  
Author(s):  
L Wagner ◽  
V Marschall ◽  
S Karl ◽  
S Cristofanon ◽  
K Zobel ◽  
...  
Keyword(s):  
Dependent Manner ◽  
Glioblastoma Cells ◽  
Smac Mimetic ◽  
Induced Apoptosis

scholarly journals NF-κB Is Required for Smac Mimetic-Mediated Sensitization of Glioblastoma Cells for γ-Irradiation–Induced Apoptosis

2011 ◽  
Vol 10 (10) ◽  
pp. 1867-1875 ◽  
Author(s):  
Rebecca Berger ◽  
Claudia Jennewein ◽  
Viola Marschall ◽  
Sabine Karl ◽  
Silvia Cristofanon ◽  
...  
Keyword(s):  
Glioblastoma Cells ◽  
Γ Irradiation ◽  
Smac Mimetic ◽  
Induced Apoptosis

scholarly journals Identification of non-canonical NF-κB signaling as a critical mediator of Smac mimetic-stimulated migration and invasion of glioblastoma cells

2013 ◽  
Vol 4 (3) ◽  
pp. e564-e564 ◽  
Author(s):  
A Tchoghandjian ◽  
C Jennewein ◽  
I Eckhardt ◽  
K Rajalingam ◽  
S Fulda
Keyword(s):  
Migration And Invasion ◽  
Glioblastoma Cells ◽  
Smac Mimetic

scholarly journals Synthesis and anti-glioblastoma effects of artemisinin-isothiocyanate derivatives

RSC Advances ◽  
2018 ◽  
Vol 8 (71) ◽  
pp. 40974-40983
Author(s):  
Chan Myae Nyein ◽  
Xiaolin Zhong ◽  
Junfeng Lu ◽  
Huijuan Luo ◽  
Jiamin Wang ◽  
...  
Keyword(s):  
Glioblastoma Cells ◽  
Cytotoxic Effects ◽  
Human Glioblastoma ◽  
Human Glioblastoma Cells ◽  
Induced Apoptosis ◽  
U87 Cells

Synthesis of artemisinin-isothiocyanate derivatives; evaluation of the cytotoxic effects of these compounds on U87 human glioblastoma cells; compound5binduced apoptosis and autophagy in U87 cells; compound5bsignificantly inhibited the migration of U87 cells.

scholarly journals Cytotoxic and Senolytic Effects of Methadone in Combination with Temozolomide in Glioblastoma Cells

2020 ◽  
Vol 21 (19) ◽  
pp. 7006
Author(s):  
Bernd Kaina ◽  
Lea Beltzig ◽  
Andrea Piee-Staffa ◽  
Bodo Haas
Keyword(s):  
Pain Treatment ◽  
Human Fibroblasts ◽  
Methadone Treatment ◽  
Fibroblast Cell ◽  
Glioblastoma Cells ◽  
First Line ◽  
Induced Apoptosis ◽  
Methadone Concentration

Methadone is an analgesic drug used for pain treatment and heroin substitution. Recently, methadone has been proposed to be useful also for cancer therapy, including glioblastoma multiforme (GBM), the most severe form of brain cancer, because experiments on cultured glioma cells treated with doxorubicin showed promising results. Doxorubicin, however, is not used first-line in GBM therapy. Therefore, we analyzed the cytotoxic effect of methadone alone and in combination with temozolomide, a DNA-alkylating drug that is first-line used in GBM treatment, utilizing GBM-derived cell lines and a human fibroblast cell line. We show that methadone is cytotoxic on its own, inducing apoptosis and necrosis, which was observed at a concentration above 20 µg/mL. Methadone was similar toxic in isogenic MGMT expressing and non-expressing cells, and in LN229 glioblastoma and VH10T human fibroblasts. The apoptosis-inducing activity of methadone is not bound on the opioid receptor (OR), since naloxone, a competitive inhibitor of OR, did not attenuate methadone-induced apoptosis/necrosis. Administrating methadone and temozolomide together, temozolomide had no impact on methadone-induced apoptosis (which occurred 3 days after treatment), while temozolomide-induced apoptosis (which occurred 5 days after treatment) was unaffected at low (non-toxic) methadone concentration (5 µg/mL), and at high (toxic) methadone concentration (20 µg/mL) the cytotoxic effects of methadone and temozolomide were additive. Methadone is not genotoxic, as revealed by comet and γH2AX assay, and did not ameliorate the genotoxic effect of temozolomide. Further, methadone did not induce cellular senescence and had no effect on temozolomide-induced senescence. Although methadone was toxic on senescent cells, it cannot be considered a senolytic drug since cytotoxicity was not specific for senescent cells. Finally, we show that methadone had no impact on the MGMT promoter methylation. Overall, the data show that methadone on glioblastoma cells in vitro is cytotoxic and induces apoptosis/necrosis at doses that are above the level that can be achieved in vivo. It is not genotoxic, and does not ameliorate the cell killing or the senescence-inducing effect of temozolomide (no synergistic effect), indicating it has no impact on temozolomide-induced signaling pathways. The data do not support the notion that concomitant methadone treatment supports temozolomide-based chemotherapy.

scholarly journals The Anti-Cancer Effect of Linusorb B3 from Flaxseed Oil through the Promotion of Apoptosis, Inhibition of Actin Polymerization, and Suppression of Src Activity in Glioblastoma Cells

Molecules ◽  
2020 ◽  
Vol 25 (24) ◽  
pp. 5881
Author(s):  
Nak Yoon Sung ◽  
Deok Jeong ◽  
Youn Young Shim ◽  
Zubair Ahmed Ratan ◽  
Young-Jin Jang ◽  
...  
Keyword(s):  
Actin Polymerization ◽  
Biological Activities ◽  
B Cell Lymphoma ◽  
Underlying Mechanism ◽  
Flaxseed Oil ◽  
C6 Cells ◽  
Glioblastoma Cells ◽  
Downstream Effector ◽  
Anti Cancer ◽  
Induced Apoptosis

Linusorbs (LOs) are natural peptides found in flaxseed oil that exert various biological activities. Of LOs, LOB3 ([1–9-NαC]-linusorb B3) was reported to have antioxidative and anti-inflammatory activities; however, its anti-cancer activity has been poorly understood. Therefore, this study investigated the anti-cancer effect of LOB3 and its underlying mechanism in glioblastoma cells. LOB3 induced apoptosis and suppressed the proliferation of C6 cells by inhibiting the expression of anti-apoptotic genes, B cell lymphoma 2 (Bcl-2) and p53, as well as promoting the activation of pro-apoptotic caspases, caspase-3 and -9. LOB3 also retarded the migration of C6 cells, which was achieved by suppressing the formation of the actin cytoskeleton critical for the progression, invasion, and metastasis of cancer. Moreover, LOB3 inhibited the activation of the proto-oncogene, Src, and the downstream effector, signal transducer and activator of transcription 3 (STAT3), in C6 cells. Taken together, these results suggest that LOB3 plays an anti-cancer role by inducing apoptosis and inhibiting the migration of C6 cells through the regulation of apoptosis-related molecules, actin polymerization, and proto-oncogenes.

scholarly journals IKKβ-mediated nuclear factor-κB activation attenuates smac mimetic–induced apoptosis in cancer cells

2009 ◽  
Vol 8 (6) ◽  
pp. 1636-1645 ◽  
Author(s):  
Lang Bai ◽  
Wenshu Chen ◽  
Wenjie Chen ◽  
Xia Wang ◽  
Hong Tang ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Smac Mimetic ◽  
Induced Apoptosis ◽  
Apoptosis In Cancer Cells
Sign in / Sign up

Export Citation Format

Share Document