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Review
. 2013 May;13(4):563-75.
doi: 10.2174/1871520611313040005.

Cell survival signaling in neuroblastoma

Michael L Megison  1 , Lauren A Gillory, Elizabeth A Beierle
Affiliations
Review

Cell survival signaling in neuroblastoma

Michael L Megison et al. Anticancer Agents Med Chem. 2013 May.

Abstract

Neuroblastoma is the most common extracranial solid tumor of childhood and is responsible for over 15% of pediatric cancer deaths. Neuroblastoma tumorigenesis and malignant transformation is driven by overexpression and dominance of cell survival pathways and a lack of normal cellular senescence or apoptosis. Therefore, manipulation of cell survival pathways may decrease the malignant potential of these tumors and provide avenues for the development of novel therapeutics. This review focuses on several facets of cell survival pathways including protein kinases (PI3K, AKT, ALK, and FAK), transcription factors (NF-κB, MYCN and p53), and growth factors (IGF, EGF, PDGF, and VEGF). Modulation of each of these factors decreases the growth or otherwise hinders the malignant potential of neuroblastoma, and many therapeutics targeting these pathways are already in the clinical trial phase of development. Continued research and discovery of effective modulators of these pathways will revolutionize the treatment of neuroblastoma.

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Figures

Figure 1
Figure 1
Immunofluorescence staining followed by confocal microscopy was employed to evaluate p53 and FAK colocalization. SK-N-AS neuroblastoma cells were stained for p53 (red, A.) and FAK (green, B.) and evaluated with confocal microscopy to determine colocalization. Merged image (C) shows colocalization of the two stains with a Manders coefficient, MA and MB of 0.68 and 0.33, respectively. D. Enlarged area of (C) (white box) to demonstrate colocalization of the two stains in the nucleus and perinuclear areas.
Figure 2
Figure 2
SH-EP neuroblastoma cells were treated with a 7-mer peptide to disrupt the p53-FAK interaction and compared to untreated cells and cells treated with the TAT sequence alone. Cell viability was measured with alamarBlue® assay. There was a significant decrease in cell viability following peptide treatment compared to either control cells or cells treated with TAT sequence alone. The TAT sequence did not significantly affect cell viability.
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