Real-Time Monitoring of Human Glioma Cell Migration on Dorsal Root Ganglion Axon-Oligodendrocyte Co-Cultures

10.3791/59744 ◽  
2019 ◽  
Author(s):  
John P. Zepecki ◽  
Kristin M. Snyder ◽  
Nikos Tapinos
Keyword(s):  
Cell Migration ◽  
Dorsal Root Ganglion ◽  
Real Time ◽  
Dorsal Root ◽  
Glioma Cell ◽  
Human Glioma ◽  
Real Time Monitoring ◽  
Human Glioma Cell ◽  
Glioma Cell Migration

scholarly journals Regulation of human glioma cell migration, tumor growth, and stemness gene expression using a Lck targeted inhibitor

Oncogene ◽  
2018 ◽  
Vol 38 (10) ◽  
pp. 1734-1750 ◽  
Author(s):  
J. P. Zepecki ◽  
K. M. Snyder ◽  
M. M. Moreno ◽  
E. Fajardo ◽  
A. Fiser ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Migration ◽  
Tumor Growth ◽  
Glioma Cell ◽  
Human Glioma ◽  
Human Glioma Cell ◽  
Glioma Cell Migration

scholarly journals Cannabidiol inhibits human glioma cell migration through a cannabinoid receptor-independent mechanism

2005 ◽  
Vol 144 (8) ◽  
pp. 1032-1036 ◽  
Author(s):  
Angelo Vaccani ◽  
Paola Massi ◽  
Arianna Colombo ◽  
Tiziana Rubino ◽  
Daniela Parolaro
Keyword(s):  
Cell Migration ◽  
Glioma Cell ◽  
Cannabinoid Receptor ◽  
Human Glioma ◽  
Human Glioma Cell ◽  
Independent Mechanism ◽  
Glioma Cell Migration

scholarly journals CSIG-35. A LOCALLY TRANSLATED Lck PATHWAY REGULATES HUMAN GLIOMA CELL MIGRATION, TUMOR GROWTH AND STEMNESS GENE EXPRESSION

2017 ◽  
Vol 19 (suppl_6) ◽  
pp. vi57-vi57
Author(s):  
John Zepecki ◽  
Kristin Snyder ◽  
Steven Toms ◽  
Atom Sarkar ◽  
Nikos Tapinos
Keyword(s):  
Gene Expression ◽  
Cell Migration ◽  
Tumor Growth ◽  
Glioma Cell ◽  
Human Glioma ◽  
Human Glioma Cell ◽  
Glioma Cell Migration

scholarly journals EXTH-03. HUMAN GLIOMA CELL MIGRATION AND INVASION PROPERTIES ARE INHIBITED BY EXPOSURE TO TUMOR TREATING FIELDS (TTFIELDS) IN VITRO

2016 ◽  
Vol 18 (suppl_6) ◽  
pp. vi60-vi60
Author(s):  
Rosa Schneiderman ◽  
Anna Shteingauz ◽  
Moshe Giladi ◽  
Tali Voloshin ◽  
Yaara Porat ◽  
...  
Keyword(s):  
Cell Migration ◽  
Glioma Cell ◽  
Migration And Invasion ◽  
Human Glioma ◽  
Cell Migration And Invasion ◽  
Human Glioma Cell ◽  
Tumor Treating Fields ◽  
Glioma Cell Migration

scholarly journals Abstract 900: Tumor Treating Fields (TTFields) affect human glioma cell migration, invasion and adherence properties in vitro

2017 ◽  
Author(s):  
Dario Garcia-Carracedo ◽  
Rosa S. Schneiderman ◽  
Einav Zeevi ◽  
Anna Shteingauz ◽  
Moshe Giladi ◽  
...  
Keyword(s):  
Cell Migration ◽  
Glioma Cell ◽  
Human Glioma ◽  
Human Glioma Cell ◽  
Tumor Treating Fields ◽  
Glioma Cell Migration

Induction of glioma cell migration by vitronectin in human serum and cerebrospinal fluid

2007 ◽  
Vol 107 (3) ◽  
pp. 578-585 ◽  
Author(s):  
Yuji Fukushima ◽  
Masakazu Tamura ◽  
Hidemitsu Nakagawa ◽  
Kazuyuki Itoh
Keyword(s):  
Cerebrospinal Fluid ◽  
Cell Migration ◽  
Healthy Volunteers ◽  
Human Serum ◽  
Glioma Cell ◽  
Glioma Cells ◽  
Heat Inactivation ◽  
Human Glioma ◽  
Human Glioma Cells ◽  
Glioma Cell Migration

Object Malignant gliomas are often highly invasive and can migrate along blood vessels. The purpose of the current study was to identify the substance in human serum and/or cerebrospinal fluid (CSF) that promotes glioma cell migration. Methods The authors used a Boyden chamber cell migration assay to study the effect of serum from patients with glioma and healthy volunteers on chemotaxis of A172 human glioma cells. Heat inactivation, trypsinization, and ultra-filtration of serum were used to establish the nature of the active factor. Vitronectin and fibronectin were chosen for further investigations; chemotactic effects were studied in both serum and CSF. Results Serum from both patients with glioma and healthy volunteers was found to promote chemotaxis of human glioma cells. This activity was greatly reduced by heat inactivation or trypsinization. Fractionation of the serum by ultrafiltration through membranes with various pore sizes showed that the active molecule was larger than 50 kD. Antibodies against integrin αv or αvβ5 or arginine-glycine-aspartic acid–containing peptides, both of which block the vitronectin–glioma cell interactions, significantly reduced serum-induced cell migration, whereas blocking the interaction of glioma cells with fibronectin had no effect. Furthermore, the ability of serum to promote the migration of A172 or T98G glioma cells was suppressed by immunodepletion of vitronectin and restored by the addition of exogenous vitronectin. The migration of glioma cells induced by CSF collected from the postoperative cavity of a malignant glioma patient was also reduced by blocking the interaction of glioma cells with vitronectin. Conclusions These results suggest that vitronectin is one of the major factors in serum- and CSF-induced glioma cell migration.

scholarly journals Targeting Aryl Hydrocarbon Receptor with small molecule, 1′H-indole-3′-carbonyl-thiazole-4-carboxylic acid methyl ester blocked human glioma cell invasion via MYH9

2020 ◽  
Author(s):  
Lijiao Zhao ◽  
Qiuting Shu ◽  
Hui Sun ◽  
Yunlong Ma ◽  
Dandan Kang ◽  
...  
Keyword(s):  
Cell Migration ◽  
Carboxylic Acid ◽  
Methyl Ester ◽  
Glioma Cell ◽  
Acid Methyl Ester ◽  
Glioma Cells ◽  
Human Glioma ◽  
Aryl Hydrocarbon ◽  
Acid Methyl ◽  
Glioma Cell Migration

AbstractAryl hydrocarbon receptor (AHR) was a master regulator of anti-tumor cell migration in various cell types. Whether and how AHR regulates glioma cell migration is largely unknown. We found that small molecule 2-(1′H-indole-3′-carbonyl)-thiazole-4-carboxylic acid methyl ester (ITE), an endogenous AHR ligand, can significantly block glioma cell migration and invasion in vitro, ex vivo and in vivo. Knocking down AHR by siRNA abolished ITE’s migration-inhibiting effects. ITE increased the number of filopodia-like protrusion formation, but reduced protrusion attachment to the extracellular matrix, and inhibited the rear retraction of migrating glioma cells. Moreover, both mesenchymal and amoeboid migrating cells were observed in the DMSO control group while none of the cells display amoeboid migration in the ITE treated group. MYH9 was significantly reduced by ITE treatment in human glioma cells. Over-expression of MYH9 abrogated ITE’s migration-inhibiting effects, with the expression level of MYH9 correlated with cell migration ability. Since MYH9 is a component of non-muscle myosin IIA (NMIIA), which is essential for cell migration in 3D confined space, and not a discovered target of AHR, the fact that ITE affects MYH9 via AHR opens a new research and development avenue.

scholarly journals MicroRNA-16 inhibits the migration and invasion of glioma cell by targeting Bcl-2 gene

2021 ◽  
Vol 19 (12) ◽  
pp. 2499-2504
Author(s):  
Baochang Luo ◽  
Jing Zhang
Keyword(s):  
Cell Migration ◽  
Immunohistochemical Staining ◽  
Glioma Cell ◽  
Scratch Test ◽  
Migration And Invasion ◽  
Invasion Assay ◽  
Human Glioma ◽  
Transwell Invasion Assay ◽  
Protein Expressions ◽  
Glioma Cell Migration

Purpose: To investigate the effect of microRNA-16 (miR-16) on glioma cell migration and invasiveness, and the mechanism involved.Methods: MicroRNA-16 mimic or inhibitor was transfected into human glioma (SHG44) cells. Cell migration, invasiveness and morphology were determined using scratch test, Transwell invasion assay, and immunohistochemical staining, respectively. Expressions of bcl-2, MMP-9 and MMP-2, and NF-κB1 proteins were measured using Western blotting.Results: Overexpression of MicroRNA-16 significantly down-regulated MMP-9 protein in SHG44 cells (p < 0.05), but MMP-2 protein expressions in the 2 groups were comparable (p > 0.05). Protein expressions of MMP-9 and NF-κB1 were significantly down-regulated in human glioma positive cells, relative to negative control.Conclusion: MiR-16 overexpression suppresses the migration and invasiveness of SHG44 cells via the regulation of NF-κB1/MMP-9 signaling pathway, and it directly targets bcl-2 gene by inhibiting its protein expression. This finding affords a new target for developing new anti-glioma drugs. Keywords: Bcl-2, Expression, Glioma, MicroRNA-16, NF-κB1signaling pathway

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