Polysialylation of the neural cell adhesion molecule: Interfering with polysialylation and migration in neuroblastoma cells

Seifert, Anja; Glanz, Dagobert; Glaubitz, Nicole; Horstkorte, Rüdiger; Bork, Kaya

doi:10.1016/j.abb.2012.04.011

Cited by 23 publications

(18 citation statements)

References 51 publications

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“…A number of studies have shown that polySia is overexpressed in many tumors, such as malignant gliomas, small cell lung cancer, and neuroblastomas, to name a few . It has been postulated that polySia enables tumor cells to remain in an undifferentiated state and therefore to exist outside of the cellular “social network” and grow irrespective of regulating factors expressed by the neighboring cells.…”

Section: Resultsmentioning

confidence: 99%

Molecular Basis of the Receptor Interactions of Polysialic Acid (polySia), polySia Mimetics, and Sulfated Polysaccharides

et al. 2016

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Polysialic acid (polySia) and polySia glycomimetic molecules support nerve cell regeneration, differentiation, and neuronal plasticity. With a combination of biophysical and biochemical methods, as well as data mining and molecular modeling techniques, it is possible to correlate specific ligand-receptor interactions with biochemical processes and in vivo studies that focus on the potential therapeutic impact of polySia, polySia glycomimetics, and sulfated polysaccharides in neuronal diseases. With this strategy, the receptor interactions of polySia and polySia mimetics can be understood on a submolecular level. As the HNK-1 glycan also enhances neuronal functions, we tested whether similar sulfated oligo- and polysaccharides from seaweed could be suitable, in addition to polySia, for finding potential new routes into patient care focusing on an improved cure for various neuronal diseases. The knowledge obtained here on the structural interplay between polySia or sulfated polysaccharides and their receptors can be exploited to develop new drugs and application routes for the treatment of neurological diseases and dysfunctions.

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Section: Resultsmentioning

confidence: 99%

Molecular Basis of the Receptor Interactions of Polysialic Acid (polySia), polySia Mimetics, and Sulfated Polysaccharides

et al. 2016

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“…Cell-surface protein polysialylation is critical for modulating synaptic adaptation for neural cells [75]. High fat diet in the mouse induces recruitment of histone lysine acetyltransferase 8 to activate transcription of polysialylation gene ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 4 ( St8sia4 ) in hypothalamus.…”

Section: 1 Molecular Pathways Of Obesity Regulated By Nutritionmentioning

confidence: 99%

An assessment of molecular pathways of obesity susceptible to nutrient, toxicant and genetically induced epigenetic perturbation

Xue

Ideraabdullah

2016

The Journal of Nutritional Biochemistry

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In recent years, the etiology of human disease has greatly improved with the inclusion of epigenetic mechanisms, in particular as a common link between environment and disease. However, for most diseases we lack a detailed interpretation of the epigenetic regulatory pathways perturbed by environment and causal mechanisms. Here, we focus on recent findings elucidating nutrient-related epigenetic changes linked to obesity. We highlight studies demonstrating that obesity is a complex disease linked to disruption of epigenetically regulated metabolic pathways in the brain, adipose tissue and liver. These pathways regulate (1) homeostatic and hedonic eating behaviors (2) adipocyte differentiation and fat accumulation, and (3) energy expenditure. By compiling these data we illustrate that obesity-related phenotypes are repeatedly linked to disruption of critical epigenetic mechanisms that regulate of key metabolic genes. These data are supported by genetic mutation of key epigenetic regulators and many of the diet induced epigenetic mechanisms of obesity are also perturbed by exposure to environmental toxicants. Identifying similarly perturbed epigenetic mechanisms in multiple experimental models of obesity strengthens the translational applications of these findings. We also discuss many of the ongoing challenges to understanding the role of environmentally-induced epigenetic pathways in obesity and suggest future studies to elucidate these roles. This assessment illustrates our current understanding of molecular pathways of obesity that are susceptible to environmental perturbation via epigenetic mechanisms. Thus, it lays the groundwork for dissecting the complex interactions between diet, genes, and toxicants that contribute to obesity and obesity-related phenotypes.

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“…The cytidine monophosphate (CMP) is a compound capable of reducing STX-mediated polysialylation of NCAM (96). In addition, migration of IMR-32 NB cells decreased after application of the sialic acid precursor ManNProp, which interferes with polysialylation (97). However, despite the inhibitory effects of CMP and N -acyl mannosamines on PSA synthesis, they are unlikely therapeutic agents due to their unfavorable physicochemical properties.…”

Section: Polysialic Acidmentioning

confidence: 99%

Glycobiology of Neuroblastoma: Impact on Tumor Behavior, Prognosis, and Therapeutic Strategies

Berois

Osinaga

2014

Front. Oncol.

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Neuroblastoma (NB), accounting for 10% of childhood cancers, exhibits aberrant cell-surface glycosylation patterns. There is evidence that changes in glycolipids and protein glycosylation pathways are associated to NB biological behavior. Polysialic acid (PSA) interferes with cellular adhesion, and correlates with NB progression and poor prognosis, as well as the expression of sialyltransferase STX, the key enzyme responsible for PSA synthesis. Galectin-1 and gangliosides, overexpressed and actively shedded by tumor cells, can modulate normal cells present in the tumor microenvironment, favoring angiogenesis and immunological escape. Different glycosyltransferases are emerging as tumor markers and potential molecular targets. Immunotherapy targeting disialoganglioside GD2 rises as an important treatment option. One anti-GD2 antibody (ch14.18), combined with IL-2 and GM-CSF, significantly improves survival for high-risk NB patients. This review summarizes our current knowledge on NB glycobiology, highlighting the molecular basis by which carbohydrates and protein–carbohydrate interactions impact on biological behavior and patient clinical outcome.

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Polysialylation of the neural cell adhesion molecule: Interfering with polysialylation and migration in neuroblastoma cells

Cited by 23 publications

References 51 publications

Molecular Basis of the Receptor Interactions of Polysialic Acid (polySia), polySia Mimetics, and Sulfated Polysaccharides

Molecular Basis of the Receptor Interactions of Polysialic Acid (polySia), polySia Mimetics, and Sulfated Polysaccharides

An assessment of molecular pathways of obesity susceptible to nutrient, toxicant and genetically induced epigenetic perturbation

Glycobiology of Neuroblastoma: Impact on Tumor Behavior, Prognosis, and Therapeutic Strategies

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