Dynamic Aspects of Neural Tumor Gangliosides

Ladisch, Stephan; Liu, Yihui

doi:10.1007/978-1-4939-1154-7_23

Cited by 3 publications

(1 citation statement)

References 42 publications

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“…108–111 In addition, the aberrant and elevated expression of gang-liosides has also been observed in many types of cancer cells, thereby promoting tumor survival. 112,113 Novel epigenetic regulatory mechanisms for GSLs will contribute to a better understanding of the pathway switch observed during neuronal differentiation of NSCs. In addition, epigenetic regulation of GSLs will provide clues underlying the pathogenic mechanisms, which are useful in developing novel strategies for disease treatment and tissue damage repair.…”

Section: Conclusion and Future Studiesmentioning

confidence: 99%

Gangliosides in Nerve Cell Specification

Itokazu

Wang

2018

Progress in Molecular Biology and Translational Science

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The central nervous system is generated from progenitor cells that are recognized as neural stem cells (NSCs). NSCs are defined as undifferentiated neural cells that are characterized by the capacity for self-renewal and multipotency. Throughout neural development, NSCs undergo proliferation, migration, and cellular differentiation, and dynamic changes are observed in the composition of carbohydrate-rich molecules, including gangliosides. Gangliosides are sialic acid-containing glycosphingolipids with essential and multifaceted functions in brain development and NSC maintenance, which reflects the complexity of brain development. Our group has pioneered research on the importance of gangliosides for growth factor receptor signaling and epigenetic regulation of ganglioside biosynthesis in NSCs. We found that GD3 is the predominant ganglioside species in NSCs (>80%) and modulates NSC proliferation by interacting with epidermal growth factor receptor signaling. In postnatal brain, GD3 is required for long-term maintenance of NSCs. Deficiency in GD3 leads to developmental and behavioral deficits, such as depression. The synthesis of GD3 is switched to the synthesis of complex, brain-type gangliosides, namely, GM1, GD1a, GD1b, and GT1b, resulting in terminal differentiation and loss of “stemness” of NSCs. In this process, GM1 is augmented by a novel GM1-modulated epigenetic gene regulation mechanism of glycosyltransferases at a later differentiation stage. Consequently, our research suggests that stage-specific gangliosides play specific roles in maintaining NSC activities and in cell fate determination.

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