L1 and NCAM adhesion molecules as signaling coreceptors in neuronal migration and process outgrowth

Schmid, Ralf S.; Maness, Patricia F.

doi:10.1016/j.conb.2008.07.015

Cited by 198 publications

(177 citation statements)

References 47 publications

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“…L1CAM was originally identified as a cell adhesion molecule in the nervous system and plays critical roles during nervous system development (Maness and Schachner, 2007;Schmid and Maness, 2008). This protein contains a cytoplasmic tail, a transmembrane domain and an extracellular domain that can interact with another L1CAM molecule through homophilic binding, or EGFR, FGFR, neuropilin-1, α5β1 and αvβ3 integrins, and a number of extracellular matrix proteins through heterophilic interaction (Maness and Schachner, 2007;Schmid and Maness, 2008;Raveh et al, 2009). L1CAM mediated intra-and inter-cellular signaling plays crucial roles in regulating cell adhesion, migration, growth, survival, and cancer cell invasion.…”

Section: Specific Cell Surface Molecules In Glioblastoma Stem Cellsmentioning

confidence: 99%

Cancer stem cells in glioblastoma—molecular signaling and therapeutic targeting

et al. 2010

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Glioblastomas (GBMs) are highly lethal primary brain tumors. Despite current therapeutic advances in other solid cancers, the treatment of these malignant gliomas remains essentially palliative. GBMs are extremely resistant to conventional radiation and chemotherapies. We and others have demonstrated that a highly tumorigenic subpopulation of cancer cells called GBM stem cells (GSCs) promotes therapeutic resistance. We also found that GSCs stimulate tumor angiogenesis by expressing elevated levels of VEGF and contribute to tumor growth, which has been translated into a useful therapeutic strategy in the treatment of recurrent or progressive GBMs. Furthermore, stem cell-like cancer cells (cancer stem cells) have been shown to promote metastasis. Although GBMs rarely metastasize beyond the central nervous system, these highly infiltrative cancers often invade into normal brain tissues preventing surgical resection, and GSCs display an aggressive invasive phenotype. These studies suggest that targeting GSCs may effectively reduce tumor recurrence and significantly improve GBM treatment. Recent studies indicate that cancer stem cells share core signaling pathways with normal somatic or embryonic stem cells, but also display critical distinctions that provide important clues into useful therapeutic targets. In this review, we summarize the current understanding and advances in glioma stem cell research, and discuss potential targeting strategies for future development of anti-GSC therapies.

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Section: Specific Cell Surface Molecules In Glioblastoma Stem Cellsmentioning

confidence: 99%

Cancer stem cells in glioblastoma—molecular signaling and therapeutic targeting

et al. 2010

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“…Another class is the calcium-dependent cadherins. Both IgCAMs and cadherins can bind homophilically, and many of the Ig-CAMs also bind heterophilically (Rougon and Hobert 2003;Schmid and Maness 2008). CAMs can be shown to promote axonal growth in vitro and different classes of neurons display preferences for different CAMs.…”

Section: Adhesive Cuesmentioning

confidence: 99%

Cellular Strategies of Axonal Pathfinding

Raper

Mason

2010

Cold Spring Harbor Perspectives in Biology

157

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Axons follow highly stereotyped and reproducible trajectories to their targets. In this review we address the properties of the first pioneer neurons to grow in the developing nervous system and what has been learned over the past several decades about the extracellular and cell surface substrata on which axons grow. We then discuss the types of guidance cues and their receptors that influence axon extension, what determines where cues are expressed, and how axons respond to the cues they encounter in their environment.T his article provides an overview of how growth cones respond to the cellular substrata and molecular cues they encounter as they extend through the developing nervous system. It elaborates on the primer by Kolodkin and TessierLavigne (2010) and touches on many of the topics covered in greater detail in the articles that follow. The first sections describe how axons extend in a directed manner, the substrata on which they grow, interactions between pioneer and follower axons, and growth cone behaviors in emerging tracts and at decision points. The subsequent sections discuss examples of specific cues, their distributions, how their distributions are determined, and how growth cones integrate multiple cues during pathfinding. AXONS EXTEND IN VIVO IN A DIRECTED MANNERThe first person to visualize the growing tips of axons, Ramon y Cajal, recognized that axons for the most part grow very efficiently towards their ultimate targets. He was a strong advocate for axons finding their way in response to chemotactic cues:"If one admits that neuroblasts are endowed with chemotactic properties, then one might also imagine that they are capable of ameboid movements, initiated by factors secreted from epithelial, neural, or mesodermal elements. As a result, their processes may be oriented in the direction of chemical gradients, and thus guided to the secreting cells" (Ramon y Cajal 1892; trans. English, 1995).This surprisingly modern outlook emphasizing directed guidance was temporarily derailed by the views of Weiss during the 1920s and 1930s. He first argued that functional specificity did not arise as a consequence of specific axonal connections (Weiss 1936), and later argued that nonspecific mechanical guidance cues play a predominant role in guiding axons and organizing them into nerves and tracts

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“…The molecular basis of radial migration of cortical neurons is a well-studied process showing prominent roles for axon guidance (20,31,32), cell adhesion (33,34), cell polarity (35,36), and cytoskeleton remodeling (28,37,38). Remarkably, knowledge about transcriptional control of genes involved in radial migration is scarce.…”

Section: Discussionmentioning

confidence: 99%

FoxO6 affects Plxna4-mediated neuronal migration during mouse cortical development

Paap

Oosterbroek

Wagemans

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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The forkhead transcription factor FoxO6 is prominently expressed during development of the murine neocortex. However, its function in cortical development is as yet unknown. We now demonstrate that cortical development is altered in FoxO6 +/− and FoxO6 −/− mice, showing migrating neurons halted in the intermediate zone. Using a FoxO6-directed siRNA approach, we substantiate the requirement of FoxO6 for a correct radial migration in the developing neocortex. Subsequent genome-wide transcriptome analysis reveals altered expression of genes involved in cell adhesion, axon guidance, and gliogenesis upon silencing of FoxO6. We then show that FoxO6 binds to DAF-16-binding elements in the Plexin A4 (Plxna4) promoter region and affects Plxna4 expression. Finally, ectopic Plxna4 expression restores radial migration in FoxO6 +/− and siRNA-mediated knockdown models. In conclusion, the presented data provide insights into the molecular mechanisms whereby transcriptional programs drive cortical development.

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L1 and NCAM adhesion molecules as signaling coreceptors in neuronal migration and process outgrowth

Cited by 198 publications

References 47 publications

Cancer stem cells in glioblastoma—molecular signaling and therapeutic targeting

Cancer stem cells in glioblastoma—molecular signaling and therapeutic targeting

Cellular Strategies of Axonal Pathfinding

FoxO6 affects Plxna4-mediated neuronal migration during mouse cortical development

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