scholarly journals Corrigendum to “Pseudolaric Acid B Induces Caspase-Dependent and Caspase-Independent Apoptosis in U87 Glioblastoma Cells”

2020 ◽  
Vol 2020 ◽  
pp. 1-1
Author(s):  
Muhammad Khan ◽  
Bin Zheng ◽  
Fei Yi ◽  
Azhar Rasul ◽  
Zhuyi Gu ◽  
...  
Keyword(s):  
Glioblastoma Cells ◽  
Pseudolaric Acid B

scholarly journals Pseudolaric Acid B Induces Caspase-Dependent and Caspase-Independent Apoptosis in U87 Glioblastoma Cells

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Muhammad Khan ◽  
Bin Zheng ◽  
Fei Yi ◽  
Azhar Rasul ◽  
Zhuyi Gu ◽  
...  
Keyword(s):  
Cell Death ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Mechanistic Study ◽  
Dependent Manner ◽  
Glioblastoma Cells ◽  
Pseudolaric Acid B ◽  
M Phase ◽  
U87 Cells

Pseudolaric acid B (PLAB) is one of the major bioactive components ofPseudolarix kaempferi. It has been reported to exhibit inhibitory effect on cell proliferation in several types of cancer cells. However, there is no report elucidating its effect on glioma cells and organ toxicityin vivo. In the present study, we found that PLAB inhibited growth of U87 glioblastoma cells in a dose-dependent manner with IC50~10 μM. Flow cytometry analysis showed that apoptotic cell death mediated by PLAB was accompanied with cell cycle arrest at G2/M phase. Using Western blot, we found that PLAB induced G2/M phase arrest by inhibiting tubulin polymerization in U87 cells. Apoptotic cell death was only partially inhibited by pancaspase inhibitor, z-VAD-fmk, which suggested that PLAB-induced apoptosis in U87 cells is partially caspase-independent. Further mechanistic study demonstrated that PLAB induced caspase-dependent apoptosis via upregulation of p53, increased level of proapoptotic protein Bax, decreased level of antiapoptotic protein Bcl-2, release of cytochrome c from mitochondria, activation of caspase-3 and proteolytic cleavage of poly (ADP-ribose) polymerase (PARP) and caspase-independent apoptosis through apoptosis inducing factor (AIF). Furthermore,in vivotoxicity study demonstrated that PLAB did not induce significant structural and biochemical changes in mouse liver and kidneys at a dose of 25 mg/kg. Therefore, PLAB may become a potential lead compound for future development of antiglioma therapy.

Deregulation of BCL2 family genes in glioblastoma cells consequent to poly(butyl cyanoacrylate) nanoparticles treatment

2019 ◽  
Vol 14 (10) ◽  
pp. 1102-1106
Author(s):  
Mahdieh Sadat Taghavi ◽  
Azim Akbarzadeh ◽  
Reza Mahdian
Keyword(s):  
Glioblastoma Cells ◽  
Bcl2 Family

Glioblastoma invasion and NMDA receptors: A novel prospect

2019 ◽  
Vol 106 (3) ◽  
pp. 250-260 ◽  
Author(s):  
DN Nandakumar ◽  
P Ramaswamy ◽  
C Prasad ◽  
D Srinivas ◽  
K Goswami
Keyword(s):  
Glutamate Receptors ◽  
Cell Lines ◽  
Intracellular Signaling ◽  
Transcript Level ◽  
Glioblastoma Cells ◽  
Invasion And Migration ◽  
Matrigel Invasion ◽  
Nmdar Activation ◽  
And Migration

Purpose Glioblastoma cells create glutamate-rich tumor microenvironment, which initiates activation of ion channels and modulates downstream intracellular signaling. N-methyl-D-aspartate receptors (NMDARs; a type of glutamate receptors) have a high affinity for glutamate. The role of NMDAR activation on invasion of glioblastoma cells and the crosstalk with α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) is yet to be explored. Main methods LN18, U251MG, and patient-derived glioblastoma cells were stimulated with NMDA to activate NMDAR glutamate receptors. The role of NMDAR activation on invasion and migration and its crosstalk with AMPAR were evaluated. Invasion and migration of glioblastoma cells were investigated by in vitro trans-well Matrigel invasion and trans-well migration assays, respectively. Expression of NMDARs and AMPARs at transcript level was evaluated by quantitative real-time polymerase chain reaction. Results We determined that NMDA stimulation leads to enhanced invasion in LN18, U251MG, and patient-derived glioblastoma cells, whereas inhibition of NMDAR using MK-801, a non-competitive antagonist of the NMDAR, significantly decreased the invasive capacity. Concordant with these findings, migration was significantly augmented by NMDAR in both cell lines. Furthermore, NMDA stimulation upregulated the expression of GluN2 and GluA1 subunits at the transcript level. Conclusions This study demonstrated the previously unexplored role of NMDAR in invasion of glioblastoma cells. Furthermore, the expression of the GluN2 subunit of NMDAR and the differential overexpression of the GluA1 subunit of AMPAR in both cell lines provide a plausible rationale of crosstalk between these calcium-permeable subunits in the glutamate-rich microenvironment of glioblastoma.

Preliminary Cytotoxic Activity of Sutherlandia frutescens and Carpobrotus edulis on Malignant glioblastoma Cells

2019 ◽  
Vol 3 (5) ◽  
pp. 175-179 ◽  
Author(s):  
Sylvester Omoruyi ◽  
◽  
Adaze Enogieru ◽  
Okobi Ekpo ◽  
◽  
...  
Keyword(s):  
Cytotoxic Activity ◽  
Glioblastoma Cells ◽  
Carpobrotus Edulis ◽  
Sutherlandia Frutescens

FOXC2 Often Overexpressed in Glioblastoma Enhances Proliferation and Invasion in Glioblastoma Cells

2014 ◽  
Vol 21 (2) ◽  
pp. 111-120 ◽  
Author(s):  
Weihua Li ◽  
Xin Fu ◽  
Rongyao Liu ◽  
Chunming Wu ◽  
Jingyang Bai ◽  
...  
Keyword(s):  
Glioblastoma Cells ◽  
Proliferation And Invasion
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