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

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

PROVIDER: PRJNA432234 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6653350.fastq.gz	Fastqsanger.gz
	SRR6653351.fastq.gz	Fastqsanger.gz
	SRR6653352.fastq.gz	Fastqsanger.gz
	SRR6653353.fastq.gz	Fastqsanger.gz
	SRR6653354.fastq.gz	Fastqsanger.gz

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

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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

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

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

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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 [HT144]

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

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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

Transcriptomic profile of melanoma clinical samples treated with BRAF and MEK- inhibitors

Project description:To analyse the RNA expression differences between melanoma tumour samples treated with BRAF and MEK-inhibitors at different time points

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Transcriptional profiles of melanoma metastases from patients responsive or resistant to BRAF/MEK inhibitor

Project description:Transcriptional profiles of formalin-fixed-paraffin-embedded melanoma metastases including pre-treatment (PRE) and post-treatment (POST) specimens from 50 patients treated with BRAF inhibitors or with BRAF and MEK inhibitors

2022-04-12 | GSE196434 | GEO

Expression data from BRAF-mutant melanoma cell lines

Project description:Melanoma cell lines were assessed for differences in gene expression patterns between the lines sensitive and resistant to BRAF and MEK inhibitor drugs. 22 BRAF-mutant melanoma cell lines were assessed for response to BRAF and MEK inhibitors in a 3 day drug treatment dose response assay. Based on the IC50, 18 lines were found to be responsive to BRAF or MEK inhibition and 4 were resistant. Normalised gene expression data generated from experimental replicate affymetrix arrays was assessed to identify differential patterns of inherent gene expression between the cell lines grouped as drug-responsive or drug-resistant. This were used to idenify specific candidate genes and pathways associated with inherent BRAF/MEK inhibitor drug resistance in melanoma cells.

2015-08-26 | E-GEOD-45558 | biostudies-arrayexpress

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

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