A distinct subset of glioma cell lines with stem cell-like properties reflects the transcriptional phenotype of glioblastomas and overexpresses CXCR4 as therapeutic target

Glia ◽  
2011 ◽  
Vol 59 (4) ◽  
pp. 590-602 ◽  
Author(s):  
Alexander Schulte ◽  
Hauke S. Günther ◽  
Heidi S. Phillips ◽  
Dirk Kemming ◽  
Tobias Martens ◽  
...  
2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Hanqing Chen ◽  
Yundi Guo ◽  
Jing Sun ◽  
Jun Dong ◽  
Qinghua Bao ◽  
...  

B7 homologue 6 (B7-H6), a newly identified member of the B7 costimulatory molecule family, is not only a crucial regulator of NK cell-mediated immune responses through binding to NKp30 but also has clinical implications due to its abnormal expression in human cancers. Here, we show that B7-H6 expression is abnormally upregulated in glioma tissue and that B7-H6 is coexpressed with stem cell marker Sox2. Intriguingly, B7-H6 was rarely detected on the surface of glioma cell lines but was abundantly expressed in glioma stem-like cells (GSLCs) that were derived from the glioma cell lines in vitro. Surprisingly, B7-H6 was the only one that was preferentially expressed in the GSLCs among the B7 family members. Functionally, knockdown of B7-H6 in GSLCs by siRNAs led to the inhibition of cell proliferation, with decrease in the expression of the oncogene Myc as well as inactivation of PI3K/Akt and ERK/MAPK signaling pathways. Moreover, we determined that three genes CBL (Casitas B-Lineage Lymphoma Proto-Oncogene), CCNT1 (Cyclin T1), and RNMT (RNA guanine-7 methyltransferase) were coexpressed with B7-H6 and c-myc in glioma tissue samples from the TCGA database and found, however that only RNMT expression was inhibited by the knockdown of B7-H6 expression in the GSLCs, suggesting the involvement of RNMT in the B7-H6/c-myc axis. Extending this to 293T cells, we observed that knocking out of B7-H6 with CRISPR-Cas9 system also suppressed cell proliferation. Thus, our findings suggest B7-H6 as a potential molecule for glioma stem cell targeted immunotherapy.


1995 ◽  
Vol 89 (2) ◽  
pp. 158-165 ◽  
Author(s):  
Martin Stanulla ◽  
Karl Welte ◽  
Martin R. Hadam ◽  
Torsten Pietsch

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Yang Gao ◽  
Hui Zheng ◽  
Liangdong Li ◽  
Changshuai Zhou ◽  
Xin Chen ◽  
...  

Kinesin superfamily protein 3C (KIF3C), a motor protein of the kinesin superfamily, is expressed in the central nervous system (CNS). Recently, several studies have suggested that KIF3C may act as a potential therapeutic target in solid tumors. However, the exact function and possible mechanism of the motor protein KIF3C in glioma remain unclear. In this study, a variety of tests including CCK-8, migration, invasion, and flow cytometry assays, and western blot were conducted to explore the role of KIF3C in glioma cell lines (U87 and U251). We found that overexpression of KIF3C in glioma cell lines promoted cell proliferation, migration, and invasion and suppressed apoptosis, while silencing of KIF3C reversed these effects. Ectopic KIF3C also increased the expression of N-cadherin, vimentin, snail, and slug to promote the epithelial-mesenchymal transition (EMT). Mechanistically, overexpression of KIF3C increased the levels of phosphatidylinositol 3-kinase (PI3K) and phosphorylated protein kinase B (p-AKT). These responses were reversed by KIF3C downregulation or AKT inhibition. Our results indicate that KIF3C promotes proliferation, migration, and invasion and inhibits apoptosis in glioma cells, possibly by activating the PI3K/AKT pathway in vitro. KIF3C might act as a potential biomarker or therapeutic target for further basic research or clinical management of glioma.


1995 ◽  
Vol 89 (2) ◽  
pp. 158-165
Author(s):  
Martin Stanulla ◽  
Karl Welte ◽  
Martin R. Hadam ◽  
Torsten Pietsch

Author(s):  
Victor Ruiz-Rodado ◽  
Adrian Lita ◽  
Tyrone Dowdy ◽  
Orieta Celiku ◽  
Alejandra Cavazos-Saldana ◽  
...  

2000 ◽  
Vol 10 (3) ◽  
pp. 159-168 ◽  
Author(s):  
Friederike Schmidt ◽  
Peter Groscurth ◽  
Johannes Dichgans ◽  
Michael Weller

2020 ◽  
pp. 1-17
Author(s):  
Oscar Abel Sánchez-Velázquez ◽  
Mireli Cortés-Rodríguez ◽  
Jorge Milán-Carrillo ◽  
Julio Montes-Ávila ◽  
Benjamín Robles-Bañuelos ◽  
...  

PLoS ONE ◽  
2016 ◽  
Vol 11 (2) ◽  
pp. e0150007 ◽  
Author(s):  
Zahra Moinfar ◽  
Hannes Dambach ◽  
Bodo Schoenebeck ◽  
Eckart Förster ◽  
Nora Prochnow ◽  
...  

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