A role for distinct cell types in determining malignancy in human neuroblastoma cell lines and tumors

Ross, Robert A.; Biedler, June L.; Spengler, Barbara A.

doi:10.1016/s0304-3835(03)00079-x

Cited by 122 publications

(134 citation statements)

References 6 publications

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“…In the present study, the effect of the PPARg ligand RGZ on two NB cell lines, which have a stromal (S) (SK-N-AS) and a neuroblast (N) (SH-SY5Y) phenotype (Ciccarone et al, 1989;Ross et al, 2003;Servidei et al, 2004), was addressed. We first demonstrated that cell proliferation was readily inhibited by RGZ in the S-type cell line, whereas this effect was less evident in the N-type cells.…”

Section: Discussionmentioning

confidence: 99%

Antineoplastic effects of rosiglitazone and PPARγ transactivation in neuroblastoma cells

et al. 2006

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Neuroblastoma (NB) is the most common extracranial solid tumour in infants. Unfortunately, most children present with advanced disease and have a poor prognosis. In the present study, we evaluated the role of the peroxisome proliferator-activated receptor γ (PPAR γ ) agonist rosiglitazone (RGZ) in two NB cell lines (SK-N-AS and SH-SY5Y), which express PPAR γ . Rosiglitazone decreased cell proliferation and viability to a greater extent in SK-N-AS than in SH-SY5Y. Furthermore, 20 μ M RGZ significantly inhibited cell adhesion, invasiveness and apoptosis in SK-N-AS, but not in SH-SY5Y. Because of the different response of SK-N-AS and SH-SY5Y cells to RGZ, the function of PPAR γ as a transcriptional activator was assessed. Noticeably, transient transcription experiments with a PPAR γ responsive element showed that RGZ induced a three-fold increase of the reporter activity in SK-N-AS, whereas no effect was observed in SH-SY5Y. The different PPAR γ activity may be likely due to the markedly lower amount of phopshorylated (i.e. inactive) protein observed in SK-N-AS. To our knowledge, this is the first demonstration that the differential response of NB cells to RGZ may be related to differences in PPAR γ transactivation. This finding indicates that PPAR γ activity may be useful to select those patients, for whom PPAR γ agonists may have a beneficial therapeutic effect.

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Section: Discussionmentioning

confidence: 99%

Antineoplastic effects of rosiglitazone and PPARγ transactivation in neuroblastoma cells

et al. 2006

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“…We chose seven different cell lines that represent a spectrum of neuroblastic tumor cell types (15). The N-type cell lines [SKN-BE(2) n and SH-SY5Y] have immature neuroblasts, a high nuclear to cytoplasmic ratio, fewer adherence to the substrate, and increased adherence to other cells.…”

Section: Transcript Changes During Ra-induced Differentiation Of Neurmentioning

confidence: 99%

The RET oncogene is a critical component of transcriptional programs associated with retinoic acid–induced differentiation in neuroblastoma

Oppenheimer¹,

Cheung²,

Gerald

2007

Molecular Cancer Therapeutics

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“…Co-expression of high levels of S100A6 together with TH in the NHO2S cell line is consistent with the I-type phenotype previously described in cultured human neuroblastoma lines. 18,19 …”

Section: Neuroblastoma-associated Genes Expressionmentioning

confidence: 99%

“…17 Human neuroblastoma cell lines have been shown to consist of a mix of different cell types including neuroblastic (N-type) cells, substrate-adherent (S-type) cells and morphologically intermediate (I-type) stem cells that display a capacity for phenotypic interconversion between both N-type and S-type lineages. 18, 19 N-type cells express high levels of neuronal markers including MYCN and tyrosine hydroxylase (TH), while S-type cells appear to be non-tumourigenic cells expressing genetic markers including S100A6 and vimentin.…”

Section: Introductionmentioning

confidence: 99%

Cell lines from MYCN transgenic murine tumours reflect the molecular and biological characteristics of human neuroblastoma

Cheng

Ford

et al. 2007

European Journal of Cancer

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Overexpression of the human MYCN oncogene driven by a tyrosine hydroxylase promoter causes tumours in transgenic mice that recapitulate the childhood cancer neuroblastoma. To establish an in vitro model to study this process, a series of isogenic cell lines were developed from these MYCN-driven murine tumours. Lines were established from tumours arising in homozygous and hemizygous MYCN transgenic mice. Hemizygous tumours gave rise to cell lines growing only in suspension. Homozygous tumours gave rise to similar suspension lines as well as morphologically distinct substrate-adherent lines characteristic of human S-type neuroblastoma cells. FISH analysis demonstrated selective MYCN transgene amplification in cell lines derived from hemizygous mice. Comparative genomic hybridisation (CGH) and fluorescence in situ hybridisation (FISH) analysis confirmed a range of neuroblastoma-associated genetic changes in the various lines, in particular, gain of regions syntenic with human 17q. These isogenic lines together with the transgenic mice thus represent valuable models for investigating the biological characteristics of aggressive neuroblastoma.

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A role for distinct cell types in determining malignancy in human neuroblastoma cell lines and tumors

Cited by 122 publications

References 6 publications

Antineoplastic effects of rosiglitazone and PPARγ transactivation in neuroblastoma cells

Antineoplastic effects of rosiglitazone and PPARγ transactivation in neuroblastoma cells

The RET oncogene is a critical component of transcriptional programs associated with retinoic acid–induced differentiation in neuroblastoma

Cell lines from MYCN transgenic murine tumours reflect the molecular and biological characteristics of human neuroblastoma

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