Heterogeneous response to the growth factors [EGF, PDGF (bb), TGF‐α, bFGF, IL‐2] on glioma spheroid growth, migration and invasion

Pedersen, Paal‐Henning; Ness, Gro Oddveig; Engebraaten, Olav; Bjerkvig, Rolf; Lillehaug, Johan R.; Lærum, Ole Didrik

doi:10.1002/ijc.2910560219

Cited by 82 publications

(40 citation statements)

References 18 publications

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“…26 Briefly, glioma cells were seeded into tissue culture flasks precoated with 1% agar (Sigma) to avoid cell attachment and cause the cells to form spheroids. After 3 days, spheroids were picked and transferred to 48-well plates where 1 spheroid/well was placed in the center of the wells.…”

Section: Cell-migration Assaymentioning

confidence: 99%

Hypoxia can induce c‐Met expression in glioma cells and enhance SF/HGF‐induced cell migration

Eckerich

Zapf

Fillbrandt

et al. 2007

Intl Journal of Cancer

120

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The c-Met receptor and its ligand scatter factor/hepatocyte growth factor (SF/HGF) are strongly overexpressed in malignant gliomas. Signaling through c-Met as well as exposure to hypoxia can stimulate glioma cell migration and invasion. In several cancer cell types, hypoxia was shown to activate the c-met promoter, which contains hypoxia inducible factor-1 (HIF-1) binding sites. We hypothesized that hypoxia might upregulate c-Met also in glioma cells. Analyzing 18 different glioblastoma cell lines and 10 glioblastoma primary cultures, we found that in 50% of both the cell lines and the primary cultures c-Met protein levels were increased following exposure to hypoxia. Upregulation of c-met in response to hypoxia was also detected at the transcriptional level. In all primary cultures and in 16 of the 18 cell lines (89%), HIF1a levels were increased by hypoxia. Transfection of siRNA against HIF-1a abgrogated the hypoxic induction of c-Met, suggesting that c-Met expression is upregulated by a HIF-1a-dependent mechanism. Hypoxia sensitized glioblastoma cell lines which showed hypoxic induction of c-Met to the motogenic effects of SF/ HGF. These findings suggest that approximately half of all human glioblastomas respond to hypoxia with an induction of c-Met, which can enhance the stimulating effect of SF/HGF on tumor cell migration. ' 2007 Wiley-Liss, Inc.

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Section: Cell-migration Assaymentioning

confidence: 99%

Hypoxia can induce c‐Met expression in glioma cells and enhance SF/HGF‐induced cell migration

Eckerich

Zapf

Fillbrandt

et al. 2007

Intl Journal of Cancer

120

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“…5 Direct consequences of increased expression of a TGF-a/EGF/EGFR autocrine or paracrine loop in glioma cells include the increased motility of glioma cells. [10][11][12] In addition, heparin-binding EGF-like growth factor (HB-EGF) has been found to be overexpressed in most human glioblastoma tissues. 13 As HB-EGF is known to promote cell-motility in wound-healing models, 7 it is reasonable to hypothesize that gliomaderived HB-EGF also influences EGFR-mediated glioma motility.…”

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confidence: 99%

Epidermal growth factor receptor-transfected bone marrow stromal cells exhibit enhanced migratory response and therapeutic potential against murine brain tumors

et al. 2005

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We have created a novel cellular vehicle for gene therapy of malignant gliomas by transfection of murine bone marrow stroma cells (MSCs) with a cDNA encoding epidermal growth factor receptor (EGFR). These cells (EGFR-MSCs) demonstrate enhanced migratory responses toward glioma-conditioned media in comparison to primary MSCs in vitro. Enhanced migration of EGFR-MSC was at least partially dependent on EGF-EGFR, PI3-, MAP kinase kinase, and MAP kinases, protein kinase C, and actin polymerization. Unlike primary MSCs, EGFR-MSCs were resistant to FasL-mediated cytotoxicity and were capable of stimulating allogeneic mixed lymphocyte reaction, suggesting EGFR-MSCs possess suitable characteristics as vehicles for brain tumor immuno-gene therapy. Following injection at various sites, including the contralateral hemisphere in the brain of syngeneic mice, EGFR-MSCs were able to migrate toward GL261 gliomas or B16 melanoma in vivo. Finally, intratumoral injection with EGFR-MSC adenovirally engineered to secrete interferon-a to intracranial GL261 resulted in significantly prolonged survival in comparison to controls. These data indicate that EGFR-MSCs may serve as attractive vehicles for infiltrating brain malignancies such as malignant gliomas.

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“…Direct consequences of increased expression of a EGF/EGFR autocrine or paracrine loop in glioma cells include the enhanced motility of glioma cells [73,74] . Moreover, EGFR has also been shown to regulate NSCs migration [75] .…”

Section: Angiogenic Cytokinesmentioning

confidence: 99%

Stem cells tropism for malignant gliomas

Zhu

2007

Neurosci. Bull.

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Abstract:Various studies have demonstrated the tremendous tropism of stem cells for malignant gliomas, making these cells a potential vehicle for delivery of therapeutic genes to disseminated glioma cells. However, little is known about the mechanisms underlying the glioma-induced tropism of stem cells. Soluble factors including chemokines or growth factors released and expressed by glioma cells at least mediate the tropism of stem cells for gliomas. Here we review the possible mechanisms of stem cells tropism for malignant gliomas.

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Heterogeneous response to the growth factors [EGF, PDGF (bb), TGF‐α, bFGF, IL‐2] on glioma spheroid growth, migration and invasion

Cited by 82 publications

References 18 publications

Hypoxia can induce c‐Met expression in glioma cells and enhance SF/HGF‐induced cell migration

Hypoxia can induce c‐Met expression in glioma cells and enhance SF/HGF‐induced cell migration

Epidermal growth factor receptor-transfected bone marrow stromal cells exhibit enhanced migratory response and therapeutic potential against murine brain tumors

Stem cells tropism for malignant gliomas

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