Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

L1CAM knockdown significantly reduces metastasis in a xenograft model of human melanoma

ABSTRACT: As L1CAM expression is associated with metastasis in melanoma patients, it could be a target for the combination therapies. We investigated the functional role of L1CAM in melanoma metastasis by the use of a xenograft model of human melanoma in mice using RNAi mediated L1CAM knockdown melanoma cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE84864 | GEO | 2016/07/27

SECONDARY ACCESSION(S): PRJNA335392

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Knockdown of L1CAM significantly reduces metastasis in a xenograft model of human melanoma: L1CAM is a potential target for anti-melanoma therapy.

Project description:Finding additional functional targets for combination therapy could improve the outcome for melanoma patients. In a spontaneous metastasis xenograft model of human melanoma a shRNA mediated knockdown of L1CAM more than sevenfold reduced the number of lung metastases after the induction of subcutaneous tumors for two human melanoma cell lines (MeWo, MV3). Whole genome expression arrays of the initially L1CAM high MeWo subcutaneous tumors revealed unchanged or downregulated genes involved in epithelial to mesenchymal transition (EMT) except an upregulation of Jagged 1, indicating a compensatory change in Notch signaling especially as Jagged 1 expression showed an increase in MeWo L1CAM metastases and Jagged 1 was expressed in metastases of the initially L1CAM low MV3 cells as well. Expression of 17 genes showed concordant regulation for L1CAM knockdown tumors of both cell lines. The changes in gene expression indicated changes in the EMT network of the melanoma cells and an increase in p53/p21 and p38 activity contributing to the reduced metastatic potential of the L1CAM knockdowns. Taken together, these data make L1CAM a highly interesting therapeutic target to prevent further metastatic spread in melanoma patients.

| S-EPMC5809060 | biostudies-literature

selenocysteine tRNA methylation promotes oxidative stress resistance in melanoma metastasis [Xenograft Human]

Project description:Oxidative stress has been shown to limit metastasis of numerous cancer types including melanoma. A specialized group of 25 proteins containing the 21st amino acid, selenocysteine, plays a central role in oxidative stress resistance, which is a key driver of metastasis. A single selenocysteine tRNA methylation, Um34, is required for the translation of several stress-related selenoproteins in a selenium-dependent manner. Herein, we characterize FTSJ1 as the Um34 methyltransferase and show that its activity is required for the Sec tRNA (tRNASec) Um34 modification. Loss of Um34 affects translation of a subset of selenoproteins and increases melanoma cell sensitivity to oxidative stress while increased Um34 levels promote oxidative stress resistance. Loss of FTSJ1 does not affect primary melanoma tumor growth but abolishes metastatic spread in vivo. Overexpression of FTSJ1 specifically increases melanoma metastasis in vivo. Our work establishes FTSJ1 as the Um34 methyltransfearse and tRNASec Um34 modification as a central regulator of oxidative stress resistance during melanoma metastasis.

2024-09-03 | GSE270976 | GEO

Melanoma experimental metastasis model

Project description:Application of a melanoma experimental metastasis model to elucidate molecular mediators of melanoma brain metastasis. Malignant melanoma frequently metastasizes to the brain. The molecular mediators of brain metastasis still remains largely unknnown. Two melanoma cell lines (opposing phenotypes in vitro: invasive/proliferative) were injected (L.V) into immune-compromised animals to generate organ-specific in vivo metastatic tumor cells and host tissue. Immunomagnetic separation was applied to separate tumor cells from host stroma. A rat model was applied to generate organ-specific profiles. Subsequently, a mouse model was applied to generate in vivo brain metastatic samples to follow altered gene expression in melanoma colonizing the brain over time. Gene expression data was collected from human and animal host-specific arrays.

2014-02-26 | E-MTAB-2065 | biostudies-arrayexpress

Melanoma Brain Metastasis Atlas

Project description:Melanoma Brain Metastasis Atlas

| PRJNA768859 | ENA

Melanoma Brain Metastasis Atlas [SlideSeq]

Project description:Melanoma Brain Metastasis Atlas [SlideSeq]

| PRJNA823928 | ENA

Pulmonary melanoma metastasis

Project description:This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/In this experiment, we have injected mice with fluorescent melanoma cells and then collected their lungs 1-3 days later and run them through a flow cytometer to separate the fluorescent cells (i.e., the melanoma cells) from the non-sluprescent cells (i.e., the lung cells) so we can sequence their transcriptomes to identify the transciptional profiles associated with pulmonary melanoma metastasis.

2014-08-20 | E-ERAD-287 | biostudies-arrayexpress

Gene Signature for Aggression of Melanoma Metastases - Melanoma Metastasis

Project description:Metastasis is the deadliest phase of cancer progression. Experimental models using immunodeficient mice have been used to gain insights into the mechanisms of metastasis. We report here the identification of a “metastasis aggressiveness gene expression signature” derived using human melanoma cells selected based on their metastatic potentials in a xenotransplant metastasis model. Comparison with expression data from human melanoma patients shows that this metastasis gene signature correlates with the aggressiveness of melanoma metastases in human patients. Many genes encoding secreted and membrane proteins are included in the signature, suggesting the importance of tumor-microenvironment interactions during metastasis. Keywords: disease state

2007-10-02 | GSE8401 | GEO

Gene Signature for Aggression of Melanoma Metastases - Melanoma Metastasis (LeiFidler)

2007-10-02 | GSE7956 | GEO

Gene Signature for Aggression of Melanoma Metastases - Melanoma Metastasis (LeiATCC)

2007-10-02 | GSE7929 | GEO

Transcription profiling of human melanoma to develop a gene signature for aggression of melanoma metastases based on a xenograft mouse model

Project description:Metastasis is the deadliest phase of cancer progression. Experimental models using immunodeficient mice have been used to gain insights into the mechanisms of metastasis. We report here the identification of a âmetastasis aggressiveness gene expression signatureâ derived using human melanoma cells selected based on their metastatic potentials in a xenotransplant metastasis model. Comparison with expression data from human melanoma patients shows that this metastasis gene signature correlates with the aggressiveness of melanoma metastases in human patients. Many genes encoding secreted and membrane proteins are included in the signature, suggesting the importance of tumor-microenvironment interactions during metastasis. Experiment Overall Design: parental cell line vs xenograft model

2008-06-15 | E-GEOD-7929 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data