Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-seq of zebrafish melanoma cells after metastatic dissemination

ABSTRACT: We report how the zebrafish melanoma cell line ZMEL1 changes after intravascular injection into 2dpf zebrafish embryos, as compared to the cells growing in vitro.

ORGANISM(S): Danio rerio

PROVIDER: GSE90143 | GEO | 2016/11/23

SECONDARY ACCESSION(S): PRJNA354577

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

RNA-seq of zebrafish ZMEL1 melanoma cells versus BRAF inhibitor resistant ZMELR1 melanoma cells

Project description:We report how the zebrafish melanoma cell line ZMEL1 changes after 4 month exposure to the BRAF inhibitor PLX4032 (1uM)

2017-01-09 | GSE93299 | GEO

Cell state diversity promotes metastasis through heterotypic cluster formation in melanoma [3D culture]

Project description:We report the gene expression differences between the zebrafish melanoma cell lines ZMEL1-PRO and ZMEL1-INV

2021-09-15 | GSE151678 | GEO

Cell state diversity promotes metastasis through heterotypic cluster formation in melanoma [2D culture]

Project description:We report the gene expression differences between the zebrafish melanoma cell lines ZMEL1-PRO and ZMEL1-INV

2021-09-15 | GSE151677 | GEO

Cell state diversity promotes metastasis through heterotypic cluster formation in melanoma [RNA-Seq]

Project description:We report single-cell gene expression profiling of the zebrafish melanoma cell lines ZMEL1-PRO and ZMEL1-INV under multiple in vitro and in vivo (zebrafish transplant) conditions

2021-09-15 | GSE152998 | GEO

Disseminated melanoma cells transdifferentiate into endothelial cells in intravascular niches at metastatic sites (Li et al. 2020, Cell Reports)

Project description:Here, we combined lineage tracing in a newly developed spontaneous metastatic mouse model of melanoma, advanced imaging and single-cell RNA-sequencing approaches to search for (patho) physiologically-relevant melanoma cellular states. We identified a population of reporter-positive melanoma cells located in intravascular niches of various metastatic organs. These intravascular metastatic cells were dormant, negative for characteristic melanoma markers and acquired endothelial cell markers.

2020-04-15 | GSE148666 | GEO

A zebrafish melanoma model reveals emergence of neural crest identity during melanoma initiation [zebrafish ChIP-seq]

Project description:We report the distribution of H3K27Ac histone marks in a zebrafish melanoma cell line and a zebrafish primary melanoma tumor with the aim of identifying super-enhancer regions and regions of interest. We also report sox10 ChIP-Seq on the same zebrafish melanoma cell line.

2016-02-01 | GSE75353 | GEO

Non-canonical EphA2 signaling is a driver of tumor-endothelial cell interactions and metastatic dissemination in BRAF inhibitor resistant melanoma

Project description:Acquired BRAF/MEK inhibitor resistance in melanoma results in a new transcriptional state associated with increased risk of metastasis. Here, we identified non-canonical EphA2 signaling as a driver of the resistance-associated metastatic state. We used mass spectrometry-based proteomic and phenotypic assays to demonstrate that the expression of active non-canonical EphA2-S897E in melanoma cells led to a mesenchymal-to-amoeboid transition (MAT) driven by Cdc42 activation. The induction of MAT promoted melanoma cell invasion, survival under shear stress, adhesion to endothelial cells under continuous flow conditions, increased permeability of endothelial cell monolayers and stimulated melanoma transendothelial cell migration. In vivo, melanoma cells expressing EphA2-S897E or active Cdc42 showed superior lung retention following tail-vain injection. Analysis of BRAF inhibitor-sensitive and -resistant melanoma cells demonstrated resistance to be associated with an MAT switch, upregulation of Cdc42 activity, increased invasion, and transendothelial migration. The drug resistant metastatic state was dependent upon histone deacetylase 8 (HDAC8) activity. Silencing of HDAC8 lead to inhibition of EphA2 and AKT phosphorylation, reduced invasion and impaired melanoma cell-endothelial cell interactions. In summary, we have demonstrated that the metastatic state associated with acquired BRAF inhibitor resistance is dependent on non-canonical EphA2 signaling, leading to increased melanoma-endothelial cell interactions and enhanced tumor dissemination.

2020-11-18 | PXD020250 | Pride

Non-canonical EphA2 signaling is a driver of tumor-endothelial cell interactions and metastatic dissemination in BRAF inhibitor resistant melanoma: Phosphoproteomics

2020-11-18 | PXD020241 | Pride

MITF and BRN2 contribute to metastatic growth after dissemination of melanoma.

Project description:Melanoma tumors are highly heterogeneous, comprising of different cell types that vary in their potential for growth and invasion. Heterogeneous expression of the Microphthalmia-associated Transcription Factor (MITF) and the POU domain transcription factor BRN2 (POU3F2) has been found in malignant melanoma. Changing expression of these transcription factors as the disease progresses has been linked to the metastatic mechanism of phenotype switching. We therefore investigated the effects of MITF and BRN2 expression in melanoma growth and metastasis. Depletion of MITF resulted in a cell population that had a slowed cell cycle progression, was less invasive in vitro and had hindered tumor and metastasis forming ability in mouse xenograft studies. BRN2 depletion left a cell population with intact proliferation and invasion in vitro; however metastatic growth was significantly reduced in the mouse xenograft model. These results suggest that the proliferative population within melanoma tumors express MITF, and both MITF and BRN2 are important for metastatic growth in vivo. This finding highlights the importance of BRN2 and MITF expression in development of melanoma metastasis.

2017-08-16 | GSE101434 | GEO

Non-canonical EphA2 signaling is a driver of tumor-endothelial cell interactions and metastatic dissemination in BRAF inhibitor resistant melanoma: Expression Proteomics

2020-11-18 | PXD020242 | Pride