Antagonistic roles of full-length N-cadherin and its soluble BMP cleavage product in neural crest delamination

Shoval, Irit; Ludwig, Andreas; Kalcheim, Chaya

doi:10.1242/dev.02742

Cited by 189 publications

(289 citation statements)

References 54 publications

Supporting

Mentioning

278

Contrasting

Order By: Relevance

“…23 Noggin inactivates BMP-4 induction of the wnt1/b-catenin pathway and in parallel of N-Cadherin expression. 46 Our experiments show that the melanoma cells as aggregates have the morphological characteristics of neural crest cells after the first step of EMT. After transplantation into the neural tube, human and mouse melanoma cells participate in neural crest cell migration.…”

Section: Noggin Inhibits An Emt-like Transition Of Melanoma Cellsmentioning

confidence: 58%

Noggin blocks invasive growth of murine B16‐F1 melanoma cells in the optic cup of the chick embryo

Busch¹,

Drews²,

Eisele³

et al. 2007

Intl Journal of Cancer

View full text Add to dashboard Cite

Melanoma cells originate from the neural crest and are characterized by high migratory potential and invasive growth. After transplantation into the neural tube of the chick embryo, melanoma cells spontaneously emigrate along the neural crest pathways without tumor formation or malignant growth. This emigration depends on the constitutive over-expression of bone morphogenetic protein-2 (BMP-2) and can be ablated by the BMP-antagonist noggin. When transplanted into the embryonic optic cup, melanoma cells invade the host tissue and form malignant tumors. Here, we asked if the invasive growth of melanoma cells in the optic cup could be influenced by BMP-2 or noggin. Mouse B16-F1 cells were grown as aggregates, treated with BMP-2 or noggin during aggregation and transplanted into the optic cup of 3-day chick embryos. After 3 days of subsequent incubation, embryos were evaluated for melanoma cell invasiveness. Immunohistochemical examination revealed that untreated and BMP-2-treated melanoma cells had grown malignantly into the host tissue. However, noggin pretreatment of the aggregates had blocked melanoma cell invasiveness and tumor formation. We conclude that invasive growth of melanoma cells in vivo is BMP-dependent and can be ablated by noggin, thus rendering noggin a promising agent for the treatment of BMP-over-expressing melanoma. ' 2007 Wiley-Liss, Inc.

show abstract

Section: Noggin Inhibits An Emt-like Transition Of Melanoma Cellsmentioning

confidence: 58%

Noggin blocks invasive growth of murine B16‐F1 melanoma cells in the optic cup of the chick embryo

Busch¹,

Drews²,

Eisele³

et al. 2007

Intl Journal of Cancer

View full text Add to dashboard Cite

show abstract

“…In situ hybridization (ISH) was performed as previously described (36). The following probes were used: chick Foxd3 (14, 15), Sim1 (17), Ednrb2 (8), Fabp7 (37), Hmx1 (9), and mouse Mitf (38) and Erbb3 (39).…”

Section: Methodsmentioning

confidence: 99%

Neural crest and Schwann cell progenitor-derived melanocytes are two spatially segregated populations similarly regulated by Foxd3

Nitzan

Pfaltzgraff

Labosky

et al. 2013

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

Self Cite

103

View full text Add to dashboard Cite

Skin melanocytes arise from two sources: either directly from neural crest progenitors or indirectly from neural crest-derived Schwann cell precursors after colonization of peripheral nerves. The relationship between these two melanocyte populations and the factors controlling their specification remains poorly understood. Direct lineage tracing reveals that neural crest and Schwann cell progenitor-derived melanocytes are differentially restricted to the epaxial and hypaxial body domains, respectively. Furthermore, although both populations are initially part of the Foxd3 lineage, hypaxial melanocytes lose Foxd3 at late stages upon separation from the nerve, whereas we recently found that epaxial melanocytes segregate earlier from Foxd3-positive neural progenitors while still residing in the dorsal neural tube. Gain-and loss-offunction experiments in avians and mice, respectively, reveal that Foxd3 is both sufficient and necessary for regulating the balance between melanocyte and Schwann cell development. In addition, Foxd3 is also sufficient to regulate the switch between neuronal and glial fates in sensory ganglia. Together, we propose that differential fate acquisition of neural crest-derived cells depends on their progressive segregation from the Foxd3-positive lineage.

show abstract

“…In neurons, N-cadherin is cleaved by ADAM10 and by PS1/γ-secretase to produce a cytoplasmic fragment of N-cadherin, N-Cad/CTF2, for example stimulated by bone morphogenic protein-4 (BMP4) [102,103]. N-Cad/ CTF2 is able to interfere with the CPB/CREB transcription complex, by binding the transcription factor CBP and inducing its proteasomal degradation.…”

Section: The Cadherin Switch and Its Consequencesmentioning

confidence: 99%

EMT, the cytoskeleton, and cancer cell invasion

Yilmaz

Christofori

2009

Cancer Metastasis Rev

1,533

1,314

View full text Add to dashboard Cite

The metastatic process, i.e. the dissemination of cancer cells throughout the body to seed secondary tumors at distant sites, requires cancer cells to leave the primary tumor and to acquire migratory and invasive capabilities. In a process of epithelial-mesenchymal transition (EMT), besides changing their adhesive repertoire, cancer cells employ developmental processes to gain migratory and invasive properties that involve a dramatic reorganization of the actin cytoskeleton and the concomitant formation of membrane protrusions required for invasive growth. The molecular processes underlying such cellular changes are still only poorly understood, and the various migratory organelles, including lamellipodia, filopodia, invadopodia and podosomes, still require a better functional and molecular characterization. Notably, direct experimental evidence linking the formation of migratory membrane protrusions and the process of EMT and tumor metastasis is still lacking. In this review, we have summarized recent novel insights into the molecular processes and players underlying EMT on one side and the formation of invasive membrane protrusions on the other side.

show abstract

Antagonistic roles of full-length N-cadherin and its soluble BMP cleavage product in neural crest delamination

Cited by 189 publications

References 54 publications

Noggin blocks invasive growth of murine B16‐F1 melanoma cells in the optic cup of the chick embryo

Noggin blocks invasive growth of murine B16‐F1 melanoma cells in the optic cup of the chick embryo

Neural crest and Schwann cell progenitor-derived melanocytes are two spatially segregated populations similarly regulated by Foxd3

EMT, the cytoskeleton, and cancer cell invasion

Contact Info

Product

Resources

About