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 Smac Mimetic-Induced Upregulation of CCL2/MCP-1 Triggers Migration and Invasion of Glioblastoma Cells and Influences the Tumor Microenvironment in a Paracrine Manner

Neoplasia ◽  
2015 ◽  
Vol 17 (6) ◽  
pp. 481-489 ◽  
Author(s):  
Carina Lindemann ◽  
Viola Marschall ◽  
Andreas Weigert ◽  
Thomas Klingebiel ◽  
Simone Fulda
Keyword(s):  
Tumor Microenvironment ◽  
Migration And Invasion ◽  
Glioblastoma Cells ◽  
Smac Mimetic

scholarly journals Jinlong capsule inhibits migration and invasion in human glioblastoma cells via the modulation of mTOR/S6 signaling pathway

2019 ◽  
Vol Volume 13 ◽  
pp. 1023-1032 ◽  
Author(s):  
Jingren Shi ◽  
Wenli Zhang ◽  
Lu He ◽  
Fanhong Kong ◽  
Meichen Pan ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Migration And Invasion ◽  
Glioblastoma Cells ◽  
Human Glioblastoma ◽  
Human Glioblastoma Cells

scholarly journals Construction of a competitive endogenous RNA network and analysis of potential regulatory axis targets in glioblastoma

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Kai Yu ◽  
Huan Yang ◽  
Qiao-li Lv ◽  
Li-chong Wang ◽  
Zi-long Tan ◽  
...  
Keyword(s):  
Gene Expression ◽  
Overall Survival ◽  
Differentially Expressed Genes ◽  
Pearson Correlation ◽  
Differentially Expressed ◽  
Migration And Invasion ◽  
Glioblastoma Cells ◽  
Network Chain ◽  
Cerna Network ◽  
Potential Marker

Abstract Background Glioblastoma is the most common primary malignant brain tumor. Because of the limited understanding of its pathogenesis, the prognosis of glioblastoma remains poor. This study was conducted to explore potential competing endogenous RNA (ceRNA) network chains and biomarkers in glioblastoma by performing integrated bioinformatics analysis. Methods Transcriptome expression data from The Cancer Genome Atlas database and Gene Expression Omnibus were analyzed to identify differentially expressed genes between glioblastoma and normal tissues. Biological pathways potentially associated with the differentially expressed genes were explored by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analysis, and a protein-protein interaction network was established using the STRING database and Cytoscape. Survival analysis using Gene Expression Profiling Interactive Analysis was based on the Kaplan–Meier curve method. A ceRNA network chain was established using the intersection method to align data from four databases (miRTarBase, miRcode, TargetScan, and lncBace2.0), and expression differences and correlations were verified by quantitative reverse-transcription polymerase chain reaction analysis and by determining the Pearson correlation coefficient. Additionally, an MTS assay and the wound-healing and transwell assays were performed to evaluate the effects of complement C1s (C1S) on the viability and migration and invasion abilities of glioblastoma cells, respectively. Results We detected 2842 differentially expressed (DE) mRNAs, 2577 DE long non-coding RNAs (lncRNAs), and 309 DE microRNAs (miRNAs) that were dysregulated in glioblastoma. The final ceRNA network consisted of six specific lncRNAs, four miRNAs, and four mRNAs. Among them, four DE mRNAs and one DE lncRNA were correlated with overall survival (p < 0.05). C1S was significantly correlated with overall survival (p= 0.015). In functional assays, knockdown of C1S inhibited the proliferation and invasion of glioblastoma cell lines. Conclusions We established four ceRNA networks that may influence the occurrence and development of glioblastoma. Among them, the MIR155HG/has-miR-129-5p/C1S axis is a potential marker and therapeutic target for glioblastoma. Knockdown of C1S inhibited the proliferation, migration, and invasion of glioblastoma cells. These findings clarify the role of the ceRNA regulatory network in glioblastoma and provide a foundation for further research.

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 Integrin αvβ3 Engagement Regulates Glucose Metabolism and Migration through Focal Adhesion Kinase (FAK) and Protein Arginine Methyltransferase 5 (PRMT5) in Glioblastoma Cells

Cancers ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1111
Author(s):  
Pulin Che ◽  
Lei Yu ◽  
Gregory K. Friedman ◽  
Meimei Wang ◽  
Xiaoxue Ke ◽  
...  
Keyword(s):  
Oxidative Phosphorylation ◽  
Focal Adhesion ◽  
Aerobic Glycolysis ◽  
Integrin Αvβ3 ◽  
Metabolic Reprogramming ◽  
Migration And Invasion ◽  
Metabolic Shift ◽  
Mitochondrial Oxidative Phosphorylation ◽  
Glioblastoma Cells ◽  
Arginine Methyltransferase

Metabolic reprogramming promotes glioblastoma cell migration and invasion. Integrin αvβ3 is one of the major integrin family members in glioblastoma multiforme cell surface mediating interactions with extracellular matrix proteins that are important for glioblastoma progression. The role of αvβ3 integrin in regulating metabolic reprogramming and its mechanism of action have not been determined in glioblastoma cells. Integrin αvβ3 engagement with osteopontin promotes glucose uptake and aerobic glycolysis, while inhibiting mitochondrial oxidative phosphorylation. Blocking or downregulation of integrin αvβ3 inhibits glucose uptake and aerobic glycolysis and promotes mitochondrial oxidative phosphorylation, resulting in decreased migration and growth in glioblastoma cells. Pharmacological inhibition of focal adhesion kinase (FAK) or downregulation of protein arginine methyltransferase 5 (PRMT5) blocks metabolic shift toward glycolysis and inhibits glioblastoma cell migration and invasion. These results support that integrin αvβ3 and osteopontin engagement plays an important role in promoting the metabolic shift toward glycolysis and inhibiting mitochondria oxidative phosphorylation in glioblastoma cells. The metabolic shift in cell energy metabolism is coupled to changes in migration, invasion, and growth, which are mediated by downstream FAK and PRMT5 in glioblastoma cells.

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