Murine neuronal progenitor cells are preferentially recruited to tumor vasculature via a4-integrin and SDF-1a dependent mechanisms

Allport, Jennifer R.; Patil, Vivek R. Shinde; Weissleder, Ralph

doi:10.4161/cbt.3.9.1036

Cited by 26 publications

(21 citation statements)

References 28 publications

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“…In addition, antibody against SF/HGF was able to block the migratory behaviour of these cells stimulated by glioma-conditioned medium. Furthermore, Allport JR et al showed tumor-targeting acivity of C17.2 in vivo and identified two other factors that are involved in this NSC homing event (Allport et al, 2004). This study showed that C17.2 cells that were transduced to express luciferase (C17.2-luc) accumulated onto tumors in mice carrying Lewis lung carcinomas.…”

Section: Tumor Inhibitionmentioning

confidence: 63%

“…This study showed that C17.2 cells that were transduced to express luciferase (C17.2-luc) accumulated onto tumors in mice carrying Lewis lung carcinomas. In vitro analysis showed that accumulation of C17.2-luc cells on tumor-derived endothelium (TEC) can be inhibited by functional blocking antibodies against SDF-1alpha and CD49d suggesting the involvement of SDF-1alpha/CXCR4 receptor and alpha4-integrin in the recruitment of C17.2-luc cells (Allport et al, 2004 (Honeth et al, 2006). Upon transplantation, these modified cells showed enhanced migration towards glioma that expressed CXCR3 ligands, IP-10 and I-TAC, in comparison with parental HiB5 cells.…”

Section: Tumor Inhibitionmentioning

confidence: 99%

See 1 more Smart Citation

Neural Stem/Progenitor Cell Clones as Models for Neural Development and Transplantation

Li¹,

Zhao²,

Shu³

et al. 2012

Neural Stem Cells and Therapy

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Section: Tumor Inhibitionmentioning

confidence: 63%

Section: Tumor Inhibitionmentioning

confidence: 99%

Neural Stem/Progenitor Cell Clones as Models for Neural Development and Transplantation

Li¹,

Zhao²,

Shu³

et al. 2012

Neural Stem Cells and Therapy

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“…Previous studies have demonstrated that high-grade gliomas secrete significant levels of SDF-1·, and that the expression of this protein and the CXCR4 receptor correlates with the histological grade and invasive capacity of these tumors, as well as tumor cell survival (35)(36)(37). SDF-1· expression by tumor-derived endothelium serves to attract the migration of NSCs (45,46). Ehtesam et al (47) demonstrated that SDF-1·/CXCR4 interactions play a functional role in gliomatropic migration of NSCs.…”

Section: Discussionmentioning

confidence: 99%

Chemokines mediate mesenchymal stem cell migration toward gliomas in vitro

Shi²,

Yu³

et al. 2010

Oncol Rep

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Abstract. Previous studies have demonstrated the tremendous tropism of mesenchymal stem cells (MSCs) for malignant gliomas, making these cells a potential vehicle for delivery of therapeutic genes to disseminated glioma cells. However, the mechanisms underlying the tropism of MSCs for gliomas remain poorly defined. It has been suggested that malignant gliomas secrete a variety of chemokines, including macrophage chemoattractant protein-1 (MCP-1) and stromal cell-derived factor-1· (SDF-1·). We isolated and cultured MSCs from rat bone marrow and found that these cells express CCR2 and CXCR4, the respective receptors for MCP-1 and SDF-1·. In vitro analysis revealed that MCP-1 and SDF-1· induce the migration of MSCs. Futhermore, neutralization data suggest that MCP-1 and SDF-1· play a role in the mediation of MSC migration toward gliomas. These results highlight the potential of these cells as a tumor targeting strategy for glioma gene therapy. IntroductionMalignant gliomas are the most prevalent type of primary brain tumor. Despite extensive surgical excision and adjuvant radio-and chemotherapy, the prognoses of patients with malignant gliomas, such as glioblastoma multiforme (GBM) or anaplastic astrocytoma, remain extremely poor (1-3). The median survival is 1 year or less for patients diagnosed with GBM and ~3 years for those diagnosed with anaplastic astrocytoma (4). This treatment resistance arises, in part, from tumor infiltration of and invasion into the surrounding brain architecture. Surgical tumor resection is almost always followed by regrowth of tumor cells residing in adjacent regions of normal brain tissue because it is impossible to eliminate successfully all tumor cells using current technologies (5-7). Single tumor cells deeply infiltrate the surrounding tissue, and are thought to be responsible for tumor relapse. New therapies should target these single tumor cells, especially those that have escaped the main tumor mass (8-10).Neural stem cells (NSCs) possess extensive tropism for experimental gliomas when administered intracranially (11,12). This characteristic of NSCs has been exploited as a tumor targeting strategy for glioma gene therapy (11)(12)(13)(14)(15)(16)(17)(18)(19)(20). Unfortunately, the acquisition of sufficient therapeutic NSCs is challenging technically, and their practical application is problematic due to ethical concerns and immunological rejection. Previously, it has been suggested that mesenchymal stem cells (MSCs) may represent an alternative source of therapeutic stem cells (21,22). In experimental brain glioma models, intracranially implanted or intravenously injected MSCs can migrate away from the injection site toward tumor beds (23-27). Additionally, gene modification of MSCs with therapeutic cytokines clearly prolongs the survival of tumorbearing animals (23,25,28,29).A better understanding of the molecular events that govern MSC homing is necessary for the development of a clinicallyapplicable tumor targeting strategy for glioma gene therapy. Certain chemokines and gro...

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“…Besides primary and immortalized NSCs/NPCs, embryonic stem cell-derived NPCs seem to have the same aptitude for glioma cell tracking (6). Moreover, NSCs are able to locate not only gliomas but also tumors of a nonneural origin, suggesting that there exist common regulators of cell trafficking probably composed of secreted factors from a tumor site and receptors present on NSCs (7,8).…”

Section: Introductionmentioning

confidence: 99%

Transmembrane Protein 18 Enhances the Tropism of Neural Stem Cells for Glioma Cells

et al. 2008

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The failure of current glioma therapies is mainly due to the ability of the tumor cells to invade extensively the surrounding healthy brain tissue, hence escaping localized treatments. Neural stem cells (NSC) are able to home in on tumor foci at sites distant from the main tumor mass, possibly enabling treatment of scattered glioma clusters. To make the strategy more effective, we performed a cDNA expression library screening to identify the candidate genes that once overexpressed would enhance the tropism of NSCs for gliomas. Here, we show that a previously unannotated gene, the one encoding transmembrane protein 18 (TMEM18), is one such gene. Overexpression of TMEM18 was seen in the current study to provide NSCs and neural precursors an increased migration capacity toward glioblastoma cells in vitro and in the rat brain. Functional inactivation of the TMEM18 gene resulted in almost complete loss of the migration activity of these cells. Thus, TMEM18 is a novel cell migration modulator. Overexpression of this protein could be favorably used in NSCbased glioma therapy. [Cancer Res 2008;68(12):4614-22]

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Murine neuronal progenitor cells are preferentially recruited to tumor vasculature via a4-integrin and SDF-1a dependent mechanisms

Cited by 26 publications

References 28 publications

Neural Stem/Progenitor Cell Clones as Models for Neural Development and Transplantation

Neural Stem/Progenitor Cell Clones as Models for Neural Development and Transplantation

Chemokines mediate mesenchymal stem cell migration toward gliomas in vitro

Transmembrane Protein 18 Enhances the Tropism of Neural Stem Cells for Glioma Cells

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