How to become neural crest: From segregation to delamination

Morales, Aixa V.; Barbas, Julio A.; Nieto, M. Ángela

doi:10.1016/j.semcdb.2005.06.003

Cited by 64 publications

(56 citation statements)

References 74 publications

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“…Surprisingly, mES cells underwent cell death on type I collagen in the same culture medium. During development, the cells require a proper environment for cell differentiation and apoptotic cell death (Gilbert and College, 2000;Morales et al, 2005), and the present findings suggest that our defined culture condition could mimic the cell differentiation process during early development in vivo.…”

Section: Discussionmentioning

confidence: 56%

Induction of neural crest cells from mouse embryonic stem cells in a serum-free monolayer culture

et al. 2010

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The neural crest (NC) is a group of cells located in the neural folds at the boundary between the neural and epidermal ectoderm. NC cells differentiate into a vast range of cells, including neural cells, smooth muscle cells, bone and cartilage cells of the maxillofacial region, and odontoblasts. The molecular mechanisms underlying NC induction during early development remain poorly understood. We previously established a defined serum-free culture condition for mouse embryonic stem (mES) cells without feeders. Here, using this defined condition, we have developed a protocol to promote mES cell differentiation into NC cells in an adherent monolayer culture. We found that adding bone morphogenetic protein (BMP)-4 together with fibroblast growth factor (FGF)-2 shifts mES cell differentiation into the NC lineage. Furthermore, we have established a cell line designated as P0-6 that is derived from the blastocysts of P0-Cre/Floxed-EGFP mice expressing EGFP in an NC-lineage-specific manner. P0-6 cells cultured using this protocol expressed EGFP. This protocol could be used to help clarify the mechanisms by which cells differentiate into the NC lineage and to assist the development of applications for clinical therapy.

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Section: Discussionmentioning

confidence: 56%

Induction of neural crest cells from mouse embryonic stem cells in a serum-free monolayer culture

et al. 2010

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“…Tumor metastasis begins with EMT, a highly conserved cellular program by which cells lose intercellular adhesion and obtain migratory and invasive capabilities [20][21][22][23]. This important process generates an aggressive tumor phenotype that leads to local metastasis via direct invasion or to distant metastasis via lymphatic and circulatory systems [24].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-495 suppresses osteosarcoma invasion and migration by targeting HSP90AA1

Xiao¹,

Wang²,

Li³

et al. 2018

Oncotarget

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MiR-495 is a tumor-suppressive microRNA that participates in tumor progression in human cancers. However, its expression and biological function in osteosarcoma remains unknown. In this study, we firstly found that miR-495 is markedly downregulated in both osteosarcoma tissues and cell lines. Then we demonstrated that miR-495 suppresses the invasion and metastasis of osteosarcoma cells in vitro through inhibiting epithelial to mesenchymal transition. Function of miR-495 in vivo was also examined in mice xenograft model and we found it significantly inhibiting the lung-metastasis of osteosarcoma cells. We also demonstrated that HSP90AA1 is a direct target of miR-495 using luciferase reporter assay and Western blot analysis. Furthermore, knockdown of HSP90AA1 can restore the increased cell invasion and migration in miR-495-knockdown cells and over expression of HSP90AA1 can neutralize the impaired metastatic ability of miR-495 mimic-treated cells. This metastasis-suppressive role of miR-495 in osteosarcoma is achieved by HSP90AA1-mediated PI3K/Akt/mTOR signaling pathway. Overall, our findings proved for the first time that miR-495 acts as a tumor suppressor in osteosarcoma and inhibits cell migration and invasion by targeting HSP90AA1, thus offering a promising therapeutic target for osteosarcoma treatment.www.impactjournals.com/oncotarget/

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“…Many of the genes involved in EMT of NC cells are transcription factors which have been also classified as proto-oncogenes contributing to cancer development (Thiery, 2003). Furthermore, motile properties as well as migration behavior of NC cells mirror the migration of cancer cells (Kuriyama and Mayor, 2008;Morales et al, 2005;Theveneau and Mayor, 2012;Dupin and Sommer, 2012). Therefore, investigation of NC migration provides a deeper understanding of the molecular machinery govering the progression and invasivnes of metastatic cancer.…”

Section: An Overview Of Nc Cell Development and The Importance Of Nc mentioning

confidence: 99%

Controlled levels of canonical Wnt signaling are required for neural crest migration

Maj

Künneke

Loresch

et al. 2016

Developmental Biology

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How to become neural crest: From segregation to delamination

Cited by 64 publications

References 74 publications

Induction of neural crest cells from mouse embryonic stem cells in a serum-free monolayer culture

Induction of neural crest cells from mouse embryonic stem cells in a serum-free monolayer culture

MicroRNA-495 suppresses osteosarcoma invasion and migration by targeting HSP90AA1

Controlled levels of canonical Wnt signaling are required for neural crest migration

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