Hepatocyte Growth Factor/Scatter Factor Promotes a Switch from E- to N-Cadherin in Chick Embryo Epiblast Cells

DeLuca, Steven; Gerhart, Jacquelyn; Cochran, Eric W.; Simak, Eileen; Blitz, Jennifer; Mattiacci-Paessler, Michelle; Knudsen, Karen A.; George‐Weinstein, Mindy

doi:10.1006/excr.1999.4577

Cited by 30 publications

(24 citation statements)

References 61 publications

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“…Our discovery is supported by studies carried out in prostate cancer cell lines DU145 (Miura et al, 2001) and LNCapFGC (Davies et al, 2001). Interestingly, the cadherin switch from E-to N-cadherin in epiblast cells can be recapitulated in vitro by treating the cells with HGF (DeLuca et al, 1999).…”

Section: Melanoma-stromal Fibroblast Interactions By Direct Contactssupporting

confidence: 54%

Function and regulation of melanoma–stromal fibroblast interactions: when seeds meet soil

et al. 2003

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Melanoma development and progression not only involve genetic and epigenetic changes that take place within the melanocytic cells, but also involve processes that are determined collectively by contextual factors including intercellular adhesions and communications. In this review, we focus on melanoma-stromal fibroblast crosstalk by direct cell-cell contact and by growth factors/ cytokines/chemokines interacting with their respective receptors. The interactions between melanoma cells and stromal fibroblasts create a context that promotes tumor growth, migration/invasion, and angiogenesis. An understanding of this process and developing new experimental and screening models are of great importance for the development of effective therapeutical strategies to treat melanoma.

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Section: Melanoma-stromal Fibroblast Interactions By Direct Contactssupporting

confidence: 54%

Function and regulation of melanoma–stromal fibroblast interactions: when seeds meet soil

et al. 2003

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“…In these conditions they undergo a switch from E-to N-cadherin expression. Such a switch was already seen in the epiblast cells of the chick embryo when the cells where treated with hepatocyte growth factor (HGF) (Deluca et al, 1999). We found indications for an autocrine HGF/c-Met loop stimulating RPE cell invasion via focal adhesion kinase (FAK).…”

Section: N-cadherin Function and Signallingmentioning

confidence: 60%

N-cadherin in the spotlight of cell-cell adhesion, differentiation, embryogenesis, invasion and signalling

Derycke

Bracke²

2004

Int. J. Dev. Biol.

361

284

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Cell migration is a process which is essential during embryonic development, throughout adult life and in some pathological conditions. Cadherins, and more specifically the neural cell adhesion molecule N-cadherin, play an important role in migration. In embryogenesis, N-cadherin is the key molecule during gastrulation and neural crest development. N-cadherin mediated contacts activate several pathways like Rho GTPases and function in tyrosine kinase signalling (for example via the fibroblast growth factor receptor). In cancer, cadherins control the balance between suppression and promotion of invasion. E-cadherin functions as an invasion suppressor and is downregulated in most carcinomas, while N-cadherin, as an invasion promoter, is frequently upregulated. Expression of N-cadherin in epithelial cells induces changes in morphology to a fibroblastic phenotype, rendering the cells more motile and invasive. However in some cancers, like osteosarcoma, N-cadherin may behave as a tumour suppressor. N-cadherin can have multiple functions: promoting adhesion or induction of migration dependent on the cellular context. KEY WORDS: N-cadherin, cancer, embryogenesis, invasion, signallingInt. J. Dev. Biol. 48: 463-476 (2004) Migration and invasionCell migration is a process that is essential during embryonic development and throughout further life. In the adult, cell migration is crucial for homeostatic processes, such as effective immune responses and repair of injured tissues. To migrate, the individual cell body must modify its shape to interact with the surrounding tissue structures. The extracellular matrix (ECM) forms a substrate, as well as a barrier for the advancing cell body. Cell migration through tissues results from a continuous cycle of interdependent steps. In general, there are five steps involved in cell migration in the ECM. First comes the protrusion of the leading edge, where growing actin filaments connect to adapter proteins and push the cell membrane in an outward direction. In a second step cell-matrix interactions and focal contacts are formed. After that, surface proteases such as matrix metalloproteinases (MMP) are recruited and focal proteolysis takes place. Then the cell contracts by actomyosin activation, and finally the tail of the cell is detached from its substrate (Friedl and Wolf, 2003).Border cells of the Drosophila melanogaster ovary are nowadays used as a model for migration. There are three recently discovered signalling pathways that control distinct aspects of migration: a global steroid-hormone signal defines the timing of migration, a highly localised cytokine signal that activates the Janus kinase-signal transducer and activator of transcription is both necessary and sufficient to induce migration, and finally, a growth factor that is analogous to platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF) contributes to guiding the cells to their destination (Montell, 2003).In embryonic morphogenesis two types of collective cell movement can ...

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“…67,68 A number of studies have shown that EMT occurs in response to growth factors. [69][70][71][72][73] The role of growth factors and cytokines in the pathogenesis of silica-induced lung carcinogenesis has been the object of earlier studies. [20][21][22][74][75][76][77] It was shown that hyperplastic type II cells present in this model are sites of active production and secretion of TGF-b1.…”

Section: Discussionmentioning

confidence: 99%

Altered expression of adhesion molecules and epithelial–mesenchymal transition in silica-induced rat lung carcinogenesis

Blanco

Vicent

Elizegi

et al. 2004

Laboratory Investigation

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Loss of the epithelial phenotype and disruption of adhesion molecules is a hallmark in the epithelialmesenchymal transition (EMT) reported in several types of cancer. Most of the studies about the relevance of adhesion and junction molecules in lung cancer have been performed using established tumors or in vitro models. The sequential molecular events leading to EMT during lung cancer progression are still not well understood. We have used a rat model for multistep lung carcinogenesis to study the status of adherens and tight junction proteins and mesenchymal markers during EMT. After silica-induced chronic inflammation, rats sequentially develop epithelial hyperplasia, preneoplastic lesions, and tumors such as adenocarcinomas and squamous cell carcinomas. In comparison with normal and hyperplastic bronchiolar epithelium and with hyperplastic alveolar type II cells, the expression levels of E-cadherin, a-catenin and b-catenin were significantly reduced in adenomatoid preneoplastic lesions and in late tumors. The loss of E-cadherin in tumors was associated with its promoter hypermethylation. a-and b-catenin dysregulation lead to cytoplasmic accumulation in some carcinomas. No nuclear b-catenin localization was found at any stage of any preneoplastic or neoplastic lesion. Zonula occludens protein-1 was markedly decreased in 66% of adenocarcinomas and in 100% squamous cell carcinomas. The mesenchymal-associated proteins N-cadherin and vimentin were analyzed as markers for EMT. N-cadherin was de novo expressed in 32% of adenocarcinomas and 33% of squamous cell carcinomas. Vimentin-positive tumor cells were found in 35% of adenocarcinomas and 88% of squamous cell carcinomas. Mesenchymal markers were absent in precursor lesions, both hyperplastic and adenomatoid. The present results show that silica-induced rat lung carcinogenesis is a good model to study EMT in vivo, and also provide in vivo evidence suggesting that the changes in cell-cell adhesion molecules are an early event in lung carcinogenesis, while EMT occurs at a later stage.

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Hepatocyte Growth Factor/Scatter Factor Promotes a Switch from E- to N-Cadherin in Chick Embryo Epiblast Cells

Cited by 30 publications

References 61 publications

Function and regulation of melanoma–stromal fibroblast interactions: when seeds meet soil

Function and regulation of melanoma–stromal fibroblast interactions: when seeds meet soil

N-cadherin in the spotlight of cell-cell adhesion, differentiation, embryogenesis, invasion and signalling

Altered expression of adhesion molecules and epithelial–mesenchymal transition in silica-induced rat lung carcinogenesis

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