A model for glioma cell migration on collagen and astrocytes

We present a model for the migration of glioma cells on substrates of collagen and astrocytes. The model is based on a cellular automaton where the various dynamical effects are introduced through adequate evolution rules. Using our model, we investigate the role of homotype and heterotype gap junction communication and show that it is possible to reproduce the corresponding experimental migration patterns. In particular, we confirm the experimental findings that inhibition of homotype gap junctions favours migration while heterotype inhibition hinders it. Moreover, the effect of heterotype gap junction inhibition dominates that of homotype inhibition.

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Laminin isoforms and their integrin receptors in glioma cell migration and invasiveness: Evidence for a role of α5-laminin(s) and α3β1 integrin

Experimental Cell Research ◽

10.1016/j.yexcr.2007.07.038 ◽

2007 ◽

Vol 313 (18) ◽

pp. 3819-3831 ◽

Cited By ~ 66

Author(s):

Tomoyuki Kawataki ◽

Tetsu Yamane ◽

Hirofumi Naganuma ◽

Patricia Rousselle ◽

Ingegerd Andurén ◽

...

Keyword(s):

Cell Migration ◽

Glioma Cell ◽

Integrin Receptors ◽

Α3β1 Integrin ◽

Glioma Cell Migration

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Role of high molecular weight extracellular matrix proteins in glioma cell migration

Neuropathology and Applied Neurobiology ◽

10.1111/j.1365-2990.1997.tb01192.x ◽

1997 ◽

Vol 23 (2) ◽

pp. 102-112 ◽

Cited By ~ 20

Author(s):

R. Mahesparan ◽

B. B. Tysnes ◽

K. Edvardsen ◽

H. K. Haugeland ◽

I. Garcia Cabrera ◽

...

Keyword(s):

Molecular Weight ◽

Extracellular Matrix ◽

Cell Migration ◽

High Molecular Weight ◽

Glioma Cell ◽

Extracellular Matrix Proteins ◽

Matrix Proteins ◽

Glioma Cell Migration

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Functional Role of Matrix gla Protein in Glioma Cell Migration

Molecular Neurobiology ◽

10.1007/s12035-017-0677-1 ◽

2017 ◽

Vol 55 (6) ◽

pp. 4624-4636 ◽

Cited By ~ 8

Author(s):

Mu-Hui Fu ◽

Chih-Yen Wang ◽

Yun-Ti Hsieh ◽

Kuan-Min Fang ◽

Shun-Fen Tzeng

Keyword(s):

Cell Migration ◽

Functional Role ◽

Glioma Cell ◽

Matrix Gla Protein ◽

Glioma Cell Migration

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

Journal of Neurosurgery ◽

10.3171/jns-07/09/0578 ◽

2007 ◽

Vol 107 (3) ◽

pp. 578-585 ◽

Cited By ~ 17

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.

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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

10.1101/2020.01.13.903674 ◽

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.

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Role of Synaptojanin 2 in Glioma Cell Migration and Invasion

Cancer Research ◽

10.1158/0008-5472.can-04-2097 ◽

2004 ◽

Vol 64 (22) ◽

pp. 8271-8275 ◽

Cited By ~ 117

Author(s):

Ya-yu Chuang ◽

Nhan L. Tran ◽

Nicole Rusk ◽

Mitsutoshi Nakada ◽

Michael E. Berens ◽

...

Keyword(s):

Cell Migration ◽

Glioma Cell ◽

Migration And Invasion ◽

Cell Migration And Invasion ◽

Glioma Cell Migration

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Possible Future Issues in the Treatment of Glioblastomas: Special Emphasis on Cell Migration and the Resistance of Migrating Glioblastoma Cells to Apoptosis

Journal of Clinical Oncology ◽

10.1200/jco.2005.03.089 ◽

2005 ◽

Vol 23 (10) ◽

pp. 2411-2422 ◽

Cited By ~ 388

Author(s):

Florence Lefranc ◽

Jacques Brotchi ◽

Robert Kiss

Keyword(s):

Cell Death ◽

Cell Migration ◽

Programmed Cell Death ◽

Signaling Pathways ◽

Glioma Cell ◽

Malignant Gliomas ◽

Glioma Cells ◽

Present Review ◽

Type I ◽

Glioma Cell Migration

Purpose The present review aims to emphasize that malignant gliomas are characterized by the diffuse invasion of distant brain tissue by a myriad of single migrating cells that exhibit decreased levels of apoptosis (programmed cell death type I), thus a resistance to cytotoxic insult. Methods The present review surveys the molecular mechanisms of migration in malignant gliomas and potential issues arising from treatments, in addition to relationships between glioma cell migration and resistance to apoptosis in terms of the molecular signaling pathways. Results Clinical and experimental data demonstrate that glioma cell migration is a complex combination of multiple molecular processes, including the alteration of tumor cell adhesion to a modified extracellular matrix, the secretion of proteases by the cells, and modifications to the actin cytoskeleton. Intracellular signaling pathways involved in the acquisition of resistance to apoptosis by migrating glioma cells concern PI3K, Akt, mTOR, NF-κB, and autophagy (programmed cell death type II). Conclusion A number of signaling pathways can be constitutively activated in migrating glioma cells, thus rendering these cells resistant to cytotoxic insults. However, these pathways are not all constitutively activated at the same time in any one glioma. Particular inhibitors should therefore only be chosen if the target is present in the tumor tissue, but this is only possible if individual patients are submitted to the molecular profiling of their tumors before undergoing any treatment to combat their migratory glioma cells. Specific antimigratory compounds should be added to conventional radio- and/or chemotherapy.

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Glioma cell migration and invasion as potential target for novel treatment strategies

Translational Neuroscience ◽

10.2478/s13380-013-0126-1 ◽

2013 ◽

Vol 4 (3) ◽

Cited By ~ 9

Author(s):

Ulrike Naumann ◽

Patrick Harter ◽

Jennifer Rubel ◽

Elena Ilina ◽

Anna-Eva Blank ◽

...

Keyword(s):

Cell Migration ◽

Glioma Cell ◽

Treatment Strategies ◽

Glioma Cells ◽

Migration And Invasion ◽

Perivascular Spaces ◽

Existing Structures ◽

Preclinical Treatment ◽

The Brain ◽

Glioma Cell Migration

AbstractDiffuse human gliomas constitute a group of most treatment-refractory tumors even if maximum treatment strategies including neurosurgical resection followed by combined radio-/chemotherapy are applied. In contrast to most other neoplasms, diffusely infiltrating gliomas invade the brain along pre-existing structures such as axonal tracts and perivascular spaces. Even in cases of early diagnosis single or small clusters of glioma cells are already encountered far away from the main tumor bulk. Complex interactions between glioma cells and the surrounding extracellular matrix and considerable changes in the cytoskeletal apparatus are prerequisites for the cellular movement of glioma cells through the brain thereby escaping from most current treatments. This review provides an overview about classical and current concepts of glioma cell migration/invasion and promising preclinical treatment approaches.

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