Expression of multiple integrins and extracellular matrix components by C6 glioma cells

Malek-Hedayat, Shahnaz; Rome, Leonard H.

doi:10.1002/jnr.490310309

Cited by 16 publications

(11 citation statements)

References 32 publications

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“…Integrins have been identified on glial cells (Aloisi et al, 1992;Geisert et al, 1991;Gladson and Cheresh, 1991;Malek-Hedayat and Rome, 1992;Tawil et al, 1993;Tawil et al, 1994;Sakaguchi and Radke, 1996) and are likely to be involved in glial cell-ECM interactions during development and at sites of brain injury. Studies on rat glia have demonstrated the importance of integrin mediated cell attachment and spreading (Tawil et al, 1993;Tawil et al, 1994).…”

Section: Discussionmentioning

confidence: 99%

Characterization of focal adhesion assembly in XR1 glial cells

Folsom

Sakaguchi

1997

Glia

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Section: Discussionmentioning

confidence: 99%

Characterization of focal adhesion assembly in XR1 glial cells

Folsom

Sakaguchi

1997

Glia

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“…Adhesion and extracellular matrix proteins expressed by C6 cells are compiled in Table 1. Increased expression of the integrins α 2 β 1 , α 3 β 1 , α 6 β 1 and α v β1 is observed immunohistochemically in astrocytoma cells, whereas α 5 β 1 is expressed de novo in glioma cell lines, including C6 (Paulus et al 1993;Malek-Hedayat and Rome 1992;Gingras et al 1995). High-grade gliomas have been shown to express α v β 3 -integrin that is the only in situ vitronectin receptor.…”

Section: Adhesion Processesmentioning

confidence: 95%

Rat C6 glioma as experimental model system for the study of glioblastoma growth and invasion

Grobben

Deyn

Slegers

2002

Cell and Tissue Research

317

247

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Infiltration of the central nervous system by neoplastic cells in patients with glioblastoma multiforme (GBM) leads to neurological dysfunction and eventually to death. The elucidation of the mechanisms underlying the aggressive nature of GBM aims at improving radio-, chemo- and gene therapy. This review is focused on the use of rat C6 glioma as an experimental model system for GBM and provides an overview of the experimental data published in the literature using this cell line in elucidating the mechanism of tumor growth, angiogenesis and invasion, and in the design and evaluation of anticancer therapies. Understanding the stages of malignant brain tumor progression requires a series of experimental approaches with a varying degree of complexity. Implantation of malignant cells into animal brain tissue closely resembles in vivo tumor growth and has the advantage over simplified models that inflammatory and vascular mechanisms are activated. However, the complexity of these models makes it difficult to identify the individual processes involved in sustained tumor growth, angiogenesis and invasion. In cell culture models, the effect of growth factors, extracellular matrix components, proteases and adhesion molecules can be investigated. The secretion of tumor-derived factors into the medium can also be analyzed when simplified models are used. This review is a compilation of experimental data focused on the characterization of tumor-related processes and on the evaluation of new therapies for the treatment of malignant glial neoplasms using rat C6 glioma as a model system.

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“…It is well-known that laminin mediates attachment and stimulates migration by a wide variety of cell types. Astrocytes and glioma cell lines are particularly responsive to laminin compared to other ECM proteins, and laminin is synthesized by astroglial cells under a variety of conditions [8,14,23,30]. If laminin plays an important role in glioma tumorigenesis and invasion within CNS neuropil which is largely devoid of laminin matrices, laminin must be deposited by glioma cells or by indigenous cells in response to glioma formation.…”

Section: Discussionmentioning

confidence: 99%

“…This inhibitory effect also inhibited C6 invasion through a basement membrane-line barrier. C6 cells express several ~1 integrin receptors [30], thus further study is required to determine which ~1 integrin heterodimer specifically mediates C6 migration. On the other hand, C6 cells also expressed the laminin receptor LBP110 and anti-LBPll0 antibody primarily interfered with cell attachment and, as a consequence, migration and invasion potential were also reduced.…”

Section: Discussionmentioning

confidence: 99%

“…Specific transmembrane receptors for laminin have been implicated in mediating cell adhesion, migration and invasion of tumor cells. Several integrin heterodimers bind laminin and ~i integrins are reported to mediate glioma interactions with ECM components including laminin [30,38]. Glioma cell adhesion to collagen, fibronectin, and vitronectin is integrin-dependent and is blocked by anti-131 integrin antibodies; in contrast, attachment to laminin is not blocked by these antibodies [15].…”

Section: Introductionmentioning

confidence: 96%

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Assessment of laminin-mediated glioma invasion in vitro and by glioma tumors engrafted within rat spinal cord

et al. 1996

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Cell motility within central nervous system (CNS) neuropil may be largely restricted yet infiltration by glioma cells is commonly observed. Glioma cells remodel nervous tissue and may assemble extracellular matrix in order to migrate. We examined the rat C6 glioma cell line for laminin expression and response in vitro and following engraftment into rat spinal cord. C6 cell cultures expressed laminin-2. C6 cells attached equally well to substrates of purified laminin-1 and laminin-2 and laminin-2-enriched C6 conditioned medium. In contrast, C6 cell migration was substantially greater on laminin-2 and C6-derived substrata than on laminin-1. Glioma cell attachment to laminin-1 and -2 was largely inhibited by antibody to the laminin receptor LBP110 and by an IKVAV peptide but not by YIGSR or control peptides. IKVAV peptide and anti-LBP110 antibodies also inhibited glioma cell invasion through synthetic basement membrane. Anti-beta 1 integrin antibody selectively inhibited cell migration and invasion on laminin-2 substrata without affecting percent cell attachment. These findings suggest C6 cell migration and invasion are promoted by autocrine release of laminin-2 and involve LPB110 and beta 1 integrin laminin receptors. A possible role for laminin-2 in CNS infiltration in vivo was examined following glioma engraftment into rat spinal cord. Engrafted C6 tumors share many histologic features of invasive human glioma. Engrafted glioma cells expressed laminin, LBP110 and beta 1 integrin antigens, indicating the molecular mechanisms of C6 motility observed in culture may contribute to glioma invasion in vivo. NMR and corroborative immunocytochemistry provided precise means to monitor tumor progression following glioma engraftment into rat spinal cord. Advantages of this glioma model are discussed regarding the assessment of anti-adhesive therapies in vivo.

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Expression of multiple integrins and extracellular matrix components by C6 glioma cells

Cited by 16 publications

References 32 publications

Characterization of focal adhesion assembly in XR1 glial cells

Characterization of focal adhesion assembly in XR1 glial cells

Rat C6 glioma as experimental model system for the study of glioblastoma growth and invasion

Assessment of laminin-mediated glioma invasion in vitro and by glioma tumors engrafted within rat spinal cord

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