E- to N-cadherin switch in melanoma is associated with decreased expression of phosphatase and tensin homolog and cancer progression

Lade-Keller, Johanne; Riber-Hansen, Rikke; Guldberg, Per; Hamilton-Dutoit, Stephen; Steiniche, Torben

doi:10.1111/bjd.12426

Cited by 57 publications

(63 citation statements)

References 34 publications

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“…These modifications may promote carcinoma cells to acquire invasion ability, which constitutes a critical step in tumor malignancy and metastasis [33, 34]. The E- to N-cadherin switch has been related to increased cell invasion, tumor progression and metastasis in melanoma and other carcinomas [30, 35–37]. …”

Section: Discussionmentioning

confidence: 99%

Histone deacetylase inhibitors induce invasion of human melanoma cells in vitro via differential regulation of N-cadherin expression and RhoA activity

et al. 2016

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BackgroundHistone deacetylase inhibitors (HDACi) exert multiple cytotoxic actions on cancer cells. Currently, different synthetic HDACi are in clinical use or clinical trials; nevertheless, since both pro-invasive and anti-invasive activities have been described, there is some controversy about the effect of HDACi on melanoma cells.MethodsMatrigel and Collagen invasion assays were performed to evaluate the effect of several HDACi (Butyrate, Trichostatin A, Valproic acid and Vorinostat) on two human melanoma cell line invasion (A375 and HT-144). The expression of N- and E-Cadherin and the activity of the RhoA GTPase were analyzed to elucidate the mechanisms involved in the HDACi activity.ResultsHDACi showed a pro-invasive effect on melanoma cells in vitro. This effect was accompanied by an up-regulation of N-cadherin expression and an inhibition of RhoA activity. Moreover, the down-regulation of N-cadherin through blocking antibodies or siRNA abrogated the pro-invasive effect of the HDACi and, additionally, the inhibition of the Rho/ROCK pathway led to an increase of melanoma cell invasion similar to that observed with the HDACi treatments.ConclusionThese results suggest a role of N-cadherin and RhoA in HDACi induced invasion and call into question the suitability of some HDACi as antitumor agents for melanoma patients.

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Section: Discussionmentioning

confidence: 99%

Histone deacetylase inhibitors induce invasion of human melanoma cells in vitro via differential regulation of N-cadherin expression and RhoA activity

et al. 2016

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“…While Mikhail et al 60 found that altered PTEN expression was correlated with tumour ulceration, no association has been shown with either disease-free60 61 or overall60––62 survival. We have recently demonstrated a strong association between reduced PTEN IHC expression and ulceration, Breslow thickness and tumour stage, as well as with a poor overall relapse-free survival in univariate analysis 36. This suggests that a reduction in PTEN expression plays an important role in melanoma genesis and in the development of melanoma metastases.…”

Section: Discussionmentioning

confidence: 92%

“…The patient cohort and tissue microarray (TMA) were as described previously 36. In brief, the TMA contained sample cores from 355 primary melanomas and 37 benign and non-dysplastic naevi (19 dermal and 18 compound naevi).…”

Section: Methodsmentioning

confidence: 99%

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Immunohistochemical analysis of molecular drivers in melanoma identifies p16 as an independent prognostic biomarker

et al. 2014

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“…Here, we will focus specifically on E-cadherin and N-cadherin’s relevance to both the NC and cancer. In many cell types including the NC, EMT has long been associated with a cadherin switch that involves decreased E-cadherin and increased N-cadherin (Araki et al, 2011; Gravdal et al, 2007; Lade-Keller et al, 2013; Scarpa et al, 2015; Wheelock et al, 2008), although the importance of this particular cadherin switch remains a point of significant debate due to the perdurance of E-cadherin post-EMT in some cases (Dady et al, 2012; Dady and Duband, 2017; Huang et al, 2016). During EMT in cancer, there is usually a similar transition entailing a downregulation of E-cadherin at cell-cell junctions and an upregulation of N-cadherin (Kuphal and Bosserhoff, 2006; Thiery, 2002), but as with the NC, there may be exceptions to this behavior (Yan et al, 2016).…”

Section: Delamination and Epithelial-mesenchymal Transition (Emt)mentioning

confidence: 99%

Neural crest and cancer: Divergent travelers on similar paths

Gallik

Treffy

Nacke

et al. 2017

Mechanisms of Development

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Neural crest cells are multipotent progenitors that dynamically interpret diverse microenvironments to migrate significant distances as a loosely associated collective and contribute to many tissues in the developing vertebrate embryo. Uncovering details of neural crest migration has helped to inform a general understanding of collective cell migration, including that which occurs during cancer metastasis. Here, we discuss several commonalities and differences of neural crest and cancer cell migration and behavior. First, we focus on some of the molecular pathways required for the initial specification and potency of neural crest cells and the roles of many of these pathways in cancer progression. We also describe epithelial-to-mesenchymal transition, which plays a critical role in initiating both neural crest migration and cancer metastasis. Finally, we evaluate studies that demonstrate myriad forms of cell-cell and cell-environment communication during neural crest and cancer collective migration to highlight the remarkable similarities in their molecular and cell biological regulation.

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E- to N-cadherin switch in melanoma is associated with decreased expression of phosphatase and tensin homolog and cancer progression

Abstract: Cadherin switch and reduced/absent PTEN expression are associated in melanoma, and both factors may play important roles in the progression of melanoma.

Cited by 57 publications

References 34 publications

Histone deacetylase inhibitors induce invasion of human melanoma cells in vitro via differential regulation of N-cadherin expression and RhoA activity

Histone deacetylase inhibitors induce invasion of human melanoma cells in vitro via differential regulation of N-cadherin expression and RhoA activity

Immunohistochemical analysis of molecular drivers in melanoma identifies p16 as an independent prognostic biomarker

Neural crest and cancer: Divergent travelers on similar paths

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