Gaussian graphical modeling reveals specific lipid correlations in glioblastoma cells

Author(s):  
Nikola S. Mueller ◽  
Jan Krumsiek ◽  
Fabian J. Theis ◽  
Christian Böhm ◽  
Anke Meyer-Bäse
Author(s):  
Laura Codazzi ◽  
Alessandro Colombi ◽  
Matteo Gianella ◽  
Raffaele Argiento ◽  
Lucia Paci ◽  
...  

2017 ◽  
Vol 161 ◽  
pp. 172-190 ◽  
Author(s):  
Kei Hirose ◽  
Hironori Fujisawa ◽  
Jun Sese

Biometrics ◽  
2012 ◽  
Vol 68 (4) ◽  
pp. 1197-1206 ◽  
Author(s):  
Hokeun Sun ◽  
Hongzhe Li

2011 ◽  
Vol 5 (1) ◽  
pp. 21 ◽  
Author(s):  
Jan Krumsiek ◽  
Karsten Suhre ◽  
Thomas Illig ◽  
Jerzy Adamski ◽  
Fabian J Theis

2006 ◽  
Vol 97 (7) ◽  
pp. 1525-1550 ◽  
Author(s):  
Masashi Miyamura ◽  
Yutaka Kano

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

2019 ◽  
Vol 106 (3) ◽  
pp. 250-260 ◽  
Author(s):  
DN Nandakumar ◽  
P Ramaswamy ◽  
C Prasad ◽  
D Srinivas ◽  
K Goswami

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.


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