Extracellular Matrix Interactions with Tumor-Progressing Cells: Tumor versus Cell Type-Specific Mechanisms

Culp, Lloyd A.; Radinsky, Robert; Lin, Wen-Chiao

doi:10.1016/b978-0-12-564498-3.50007-8

Biochemical and Molecular Aspects of Selected Cancers 1991

DOI: 10.1016/b978-0-12-564498-3.50007-8

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Extracellular Matrix Interactions with Tumor-Progressing Cells: Tumor versus Cell Type-Specific Mechanisms

Lloyd A. Culp

Robert Radinsky

Wen-Chiao Lin

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1992

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Cited by 4 publications

(1 citation statement)

References 142 publications

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“…Analyses of extracellular matrix adhesion of neuroblastoma cells in culture revealed mechanisms distinct from those seen in many other cell types. Neuroblastoma cells recognise sequences on fibronectin different from most untransformed cells that have conventional integrin and heparan sulphate proteoglycan receptors (Mugnai et al, 1988;Culp & Barletta, 1990;Culp et al, 1991). These tumour cells can be missing many of the common integrin subunits (Favrot et al, 1991;Yoshihara et al, 1991Yoshihara et al, , 1992 and in other cases have a unique form of the PI subunit (Dedhar & Gray, 1990).…”

mentioning

confidence: 99%

Tumour progression of human neuroblastoma cells tagged with a lacZ marker gene: earliest events at ectopic injection sites

Kleinman

Lewandowska²,

Culp³

1994

Br J Cancer

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mentioning

confidence: 99%

Tumour progression of human neuroblastoma cells tagged with a lacZ marker gene: earliest events at ectopic injection sites

Kleinman

Lewandowska²,

Culp³

1994

Br J Cancer

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Cell‐Type‐Specific adhesion mechanisms mediated by fibronectin adsorbed to chemically derivatized substrata

Lewandowska

Pergament

Sukenik

et al. 1992

J. Biomed. Mater. Res.

122

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Plasma fibronectin (pFN) adhesion mechanisms on inert substrata were evaluated for murine fibroblasts (3T3) and human neuroblastoma (Platt) cells using glass coverslips chemically derivatized with a self-assembled monolayer of aliphatic chains terminated with a specific endgroup to interact with adsorbed pFN: [CH3], [SH], [SCOCH3], [NH2], [SO3H], or underivatized glass [SiOH]. All surfaces bound similar amounts of pFN and facilitated attachment of both cell types within narrow ranges. However, spreading/differentiation responses of cells differed considerably among the surfaces. While 3T3 cells spread and developed microfilament stress fibers comparably on all surfaces, inclusion of an RGDS-containing synthetic peptide in the medium revealed variation in resistance to stress fiber formation mediated by an RGDS-recognizing integrin: [NH2] greater than [CH3] much greater than [SiOH],[SH],[SCOCH3]. Different patterns of neurite formation were observed for neuroblastoma cells: [SiOH], [SO3H] greater than [SCOCH3],[SH] much greater than [CH3] greater than [NH2]. Similarity in cell responses to both [CH3] and [NH2] surfaces argues against a pattern dependent upon the hydrophobicity of substrata. When pFN was diluted to a subsaturable concentration with albumin for adsorption, neuroblastoma responses changed significantly from those observed on pFN-saturated surfaces, for both spreading and neurite generation: [NH2],[SO3H] much greater than [SH], [SCOCH3] greater than [SiOH],[CH3]. Responses to the pFN: albumin mixture were markedly improved from responses after sequential adsorptions, demonstrating "optimization" of pFN conformation (not merely binding) by coadsorption of albumin molecules. In most cases, the [NH2] surface yielded responses distinctively different from the other surfaces. Overall, these data suggest many variations in the conformation of pFN molecules adsorbed to specific inert surfaces, as well as variations in the responses of cell surface receptors to conformationally specific pFNs. They also reveal cell-type-specific changes in differentiated cell responses on derivatized substrata, mediated by different classes of cell surface receptors for the two cell types, and provide optimism for regulating FN-dependent adhesion mechanisms in either positive or negative contexts on biomaterial surfaces derivatized with one or more of these chemical end-groups.

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Inverse expressions of the N-myc oncogene and ?1 integrin in human neuroblastoma: relationships to disease progression in a nude mouse model system

1995

Self Cite

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A nude mouse model for human neuroblastoma has been developed to examine possible relationships between amplification/over-expression of the N-myc oncogene and altered regulation of expression of specific integrin subunits during tumor progression. Subcutaneous (ectopic) or intra-adrenal (orthotopic) injection of the neuroblastoma cell lines SK-N-SH or IMR-32 has generated a number of derivative tumor cell lines. Tumor cell lines derived from SK-N-SH cells (which do not express N-myc) or IMR-32 cells (which over-express N-myc) produce tumors at higher rates when re-injected into the subcutaneous space of nude mice. Moreover, cell lines derived from tumors initiated by IMR-32 cells exhibit shorter latent periods than do IMR-32 cells direct from tissue culture. With regard to integrin subunit expression, SK-N-SH and related cell lines express high levels of beta 1 integrin, which is associated with the alpha 2 and alpha 3 integrin subunits (predominantly alpha 3). IMR-32 cells display reduced beta 1 expression, and that which is produced is not associated with common alpha subunits. LaN1 cells, which express N-myc at even higher levels than do IMR-32 cells, express even less beta 1. Interestingly, the tumor-derived cell lines (especially those from tumors initiated in adrenal glands) also exhibit reduced integrin expression compared with the parental cell lines; this reduction is associated with the enhanced tumor take rate observed when the cells are re-injected into nude mice. Our results raise the possibility of a relationship between over-expression of N-myc and down-regulation of beta 1 integrin expression (possibly some alpha subunits also). In addition, the data suggest that human neuroblastoma-derived cell lines which exhibit reduced integrin expression display more aggressive tumor growth in nude mice.

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Extracellular Matrix Interactions with Tumor-Progressing Cells: Tumor versus Cell Type-Specific Mechanisms

Cited by 4 publications

References 142 publications

Tumour progression of human neuroblastoma cells tagged with a lacZ marker gene: earliest events at ectopic injection sites

Tumour progression of human neuroblastoma cells tagged with a lacZ marker gene: earliest events at ectopic injection sites

Cell‐Type‐Specific adhesion mechanisms mediated by fibronectin adsorbed to chemically derivatized substrata

Inverse expressions of the N-myc oncogene and ?1 integrin in human neuroblastoma: relationships to disease progression in a nude mouse model system

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