scholarly journals MicroRNA-559 Plays an Inhibitory Role in the Malignant Progression of Glioblastoma Cells by Directly Targeting Metadherin [Retraction]

2021 ◽  
Vol Volume 14 ◽  
pp. 4899-4900
Author(s):  
Fan Yang ◽  
Chuangang Zhang ◽  
Congbin Xu ◽  
Fangyou Fu ◽  
Dong Han ◽  
...  
2019 ◽  
Vol Volume 12 ◽  
pp. 4415-4426 ◽  
Author(s):  
Fan Yang ◽  
Chuangang Zhang ◽  
Congbin Xu ◽  
Fangyou Fu ◽  
Dong Han ◽  
...  

2020 ◽  
Vol 11 (2) ◽  
Author(s):  
Rui Su ◽  
Jun Ma ◽  
Jian Zheng ◽  
Xiaobai Liu ◽  
Yunhui Liu ◽  
...  

Open Medicine ◽  
2020 ◽  
Vol 15 (1) ◽  
pp. 872-881
Author(s):  
Guo-Hua Wang ◽  
Liang-Yan Wang ◽  
Cui Zhang ◽  
Peng Zhang ◽  
Chuan-Hui Wang ◽  
...  

AbstractThis study attempted to research the molecular mechanism underlying the inhibitory role of miR-1225-5p in the malignant progression of glioblastoma. Bioinformatics analyses based on the gene expression omnibus (GEO) and Chinese glioma genome atlas (CGGA) databases showed that miR-1225-5p, as a favorable prognostic factor, was expressed at low levels in glioblastoma, and its expression was also related to WHO grade and age. The subsequent CCK-8 assay indicated that miR-1225-5p might prevent the malignant progression of glioblastoma, which was represented by that miR-1225-5p mimic reduced the viability of glioblastoma cells. Then, we predicted that FNDC3B might be a potential target gene of miR-1225-5p, and it was negatively correlated with the level of miR-1225-5p, which were confirmed by dual-luciferase reporter assay, qRT-PCR and western blot assays. Moreover, based on the analyses of the cancer genome atlas (TCGA), Oncomine and CGGA databases, FNDC3B was enriched in glioblastoma and high expression of FNDC3B led to poor prognosis. Finally, CCK8 and transwell experiments showed that the ability of miR-1225-5p to inhibit glioblastoma cell viability, invasion and migration was at least partially achieved by targeting FNDC3B. In general, these results revealed that the miR-1225-5p/FNDC3B axis contributes to inhibiting the malignant phenotype of glioblastoma cells, which lays a foundation for molecular diagnosis and treatment of glioblastoma.


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.


2019 ◽  
Vol 3 (5) ◽  
pp. 175-179 ◽  
Author(s):  
Sylvester Omoruyi ◽  
◽  
Adaze Enogieru ◽  
Okobi Ekpo ◽  
◽  
...  

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