Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression analysis of human melanoma short-term culture WM451-Lu harvested after lentiviral infection with a GFP (control) or SETDB1 (experimental) viral vector

ABSTRACT: Investigation of expression differences induced by expression of the histone methyltransferase SETDB1 in human melanoma short-term culture WM451-Lu. A six-chip study using total RNA prepared from WM451-Lu melanoma short-term cultures infected with either a lentivirus encoding GFP (control) or SETDB1. Cells were allowed to grow for 2 days post-infection.

ORGANISM(S): Homo sapiens

SUBMITTER: Yariv Houvras

PROVIDER: E-GEOD-26371 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

The histone methyltransferase SETDB1 is recurrently amplified in melanoma and accelerates its onset.

Ceol Craig J CJ Houvras Yariv Y Jane-Valbuena Judit J Bilodeau Steve S Orlando David A DA Battisti Valentine V Fritsch Lauriane L Lin William M WM Hollmann Travis J TJ Ferré Fabrizio F Bourque Caitlin C Burke Christopher J CJ Turner Laura L Uong Audrey A Johnson Laura A LA Beroukhim Rameen R Mermel Craig H CH Loda Massimo M Ait-Si-Ali Slimane S Garraway Levi A LA Young Richard A RA Zon Leonard I LI

Nature 20110301 7339

The most common mutation in human melanoma, BRAF(V600E), activates the serine/threonine kinase BRAF and causes excessive activity in the mitogen-activated protein kinase pathway. BRAF(V600E) mutations are also present in benign melanocytic naevi, highlighting the importance of additional genetic alterations in the genesis of malignant tumours. Such changes include recurrent copy number variations that result in the amplification of oncogenes. For certain amplifications, the large number of genes ...[more]

PMID: 21430779

Similar Datasets

Expression analysis of melanoma harvested after GFP or SETDB1 expression

Project description:This SuperSeries is composed of the following subset Series: GSE21505: Expression analysis of melanoma harvested from GFP versus SETDB1 transgenic zebrafish (Danio rerio) GSE26371: Expression analysis of human melanoma short-term culture WM451-Lu harvested after lentiviral infection with a GFP (control) or SETDB1 (experimental) viral vector Refer to individual Series

2011-01-07 | E-GEOD-26372 | biostudies-arrayexpress

Expression analysis of human melanoma short-term culture WM451-Lu harvested after lentiviral infection with a GFP (control) or SETDB1 (experimental) viral vector

Project description:Investigation of expression differences induced by expression of the histone methyltransferase SETDB1 in human melanoma short-term culture WM451-Lu.

2011-01-07 | GSE26371 | GEO

Recurrent amplifications of the histone methyltransferase SETDB1 in melanoma

Project description:The most common mutation in human melanoma, BRAF(V600E), activates the serine/threonine kinase BRAF and causes excessive activity in the mitogen-activated protein kinase pathway. BRAF(V600E) mutations are also present in benign melanocytic naevi, highlighting the importance of additional genetic alterations in the genesis of malignant tumours. Such changes include recurrent copy number variations that result in the amplification of oncogenes. For certain amplifications, the large number of genes in the interval has precluded an understanding of the cooperating oncogenic events. Here we have used a zebrafish melanoma model to test genes in a recurrently amplified region of chromosome 1 for the ability to cooperate with BRAF(V600E) and accelerate melanoma. SETDB1, an enzyme that methylates histone H3 on lysine 9 (H3K9), was found to accelerate melanoma formation significantly in zebrafish. Chromatin immunoprecipitation coupled with massively parallel DNA sequencing and gene expression analyses uncovered genes, including HOX genes, that are transcriptionally dysregulated in response to increased levels of SETDB1. Our studies establish SETDB1 as an oncogene in melanoma and underscore the role of chromatin factors in regulating tumorigenesis. DNA was enriched from short-term cultures of cells and chromatin immunoprecipitations (ChIPs) were analyzed by Solexa sequencing. ChIPs were performed using an antibody against SetDB1 in WM853.2. Whole cell extracts are provided for WM262, WM451Lu and WM853.2 cells.

2012-03-17 | E-GEOD-36579 | biostudies-arrayexpress

The histone methyltransferase SETDB1 is recurrently amplified in melanoma and accelerates its onset

Project description:The most common mutation in human melanoma, BRAF(V600E), activates the serine/threonine kinase BRAF and causes excessive activity in the mitogen-activated protein kinase pathway. BRAF(V600E) mutations are also present in benign melanocytic naevi, highlighting the importance of additional genetic alterations in the genesis of malignant tumours. Such changes include recurrent copy number variations that result in the amplification of oncogenes. For certain amplifications, the large number of genes in the interval has precluded an understanding of the cooperating oncogenic events. Here we have used a zebrafish melanoma model to test genes in a recurrently amplified region of chromosome 1 for the ability to cooperate with BRAF(V600E) and accelerate melanoma. SETDB1, an enzyme that methylates histone H3 on lysine 9 (H3K9), was found to accelerate melanoma formation significantly in zebrafish. Chromatin immunoprecipitation coupled with massively parallel DNA sequencing and gene expression analyses uncovered genes, including HOX genes, that are transcriptionally dysregulated in response to increased levels of SETDB1. Our studies establish SETDB1 as an oncogene in melanoma and underscore the role of chromatin factors in regulating tumorigenesis. ChIP was performed from short-term cultures of WM262 and WM451Lu cells.

2011-03-25 | E-GEOD-28170 | biostudies-arrayexpress

The histone methyltransferase SETDB1 contributes to melanoma tumorigenesis and serves as a new potential therapeutic target in BRAF/MEK inhibitor-resistant melanoma [SETDB1]

Project description:The aim of this work is to establish the impact of SETDB1 expression in melanoma. SETDB1 was overexpressed in melanoma cell lines (SETDB1 OE) and whole-genome expression profiles were compared to the control ( melanoma cells carrying an empty vector). .

2019-12-31 | GSE109670 | GEO

Setdb1-loss induces type-I interferons and immune clearance of melanoma (scRNA-Seq)

Project description:Despite recent advances in the treatment of melanoma, many patients with metastatic disease still succumb to their disease. To identify tumor-intrinsic modulators of immunity to melanoma, we performed a whole-genome CRISPR screen in melanoma and identified multiple components of the HUSH complex, including Setdb1, as hits. We found that loss of Setdb1 leads to increased immunogenicity and complete tumor clearance in a CD8+ T-cell dependent manner. Mechanistically, loss of Setdb1 causes de-repression of endogenous retroviruses (ERVs) in melanoma cells and triggers tumor-cell intrinsic type-I interferon signaling, upregulation of MHC-I expression, and increased CD8+ T-cell infiltration. Furthermore, spontaneous immune clearance observed in Setdb1-/- tumors results in subsequent protection from other ERV-expressing tumor lines, supporting the functional anti-tumor role of ERV-specific CD8+ T-cells found in the Setdb1-/- microenvironment. Blocking the type-I interferon receptor in mice grafted with Setdb1-/- tumors decreases immunogenicity by decreasing MHC-I expression, leading to decreased T-cell infiltration and increased melanoma growth comparable to Setdb1wt tumors. Together, these results indicate a critical role for Setdb1 and type-I interferons in generating an inflamed tumor microenvironment, and potentiating tumor-cell intrinsic immunogenicity in melanoma. This study further emphasizes regulators of ERV expression and type-I interferon expression as potential therapeutic targets for augmenting anti-cancer immune responses.

2023-12-31 | GSE232413 | GEO

Setdb1-loss induces type-I interferons and immune clearance of melanoma (RNA-Seq)

2023-12-31 | GSE232411 | GEO

E-GEOD-26371

Project description:Expression analysis of human melanoma short-term culture WM451-Lu harvested after lentiviral infection with a GFP (control) or SETDB1 (experimental) viral vector

2015-08-12 | E-GEOD-26371 | ExpressionAtlas

The histone methyltransferase SETDB1 contributes to melanoma tumorigenesis and serves as a new potential therapeutic target in BRAF/MEK inhibitor-resistant melanoma [HT144]

2019-12-31 | GSE109669 | GEO

The histone methyltransferase SETDB1 contributes to melanoma tumorigenesis and serves as a new potential therapeutic target in BRAF/MEK inhibitor-resistant melanoma [ChIP-seq]

Project description:Histone modifications play a crucial role in the progression of various cancers. The histone methyltransferase SETDB1 catalyzes the addition of methyl groups to histone H3 at lysine 9. Here, we describe SETDB1 contribution to melanoma tumorigenesis. SETDB1 is highly amplified in melanoma cells and in patients’ tumors. Increased SETDB1 expression, which correlates with SETDB1 amplification, is associated with a more aggressive phenotype in in vitro and in vivo studies. SETDB1 implements its effects through the regulation of Thrombospondin 1. SETDB1’s SET-domain is essential to maintain its tumorigenic effects. SETDB1 inhibition reduces cell growth in melanomas resistant to targeted treatments. In essence, we support SETDB1 as a major driver of melanoma development, highlighting a role as potential future target for the treatment of this disease.

2019-12-31 | GSE109880 | GEO

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