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Homo sapiens

ABSTRACT: A zebrafish melanoma model reveals emergence of neural crest identity during melanoma initiation [human cell line ChIP-seq]

PROVIDER: PRJNA304004 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR2959430.fastq.gz	Fastqsanger.gz
	SRR2959431.fastq.gz	Fastqsanger.gz
	SRR2959432.fastq.gz	Fastqsanger.gz
	SRR2959433.fastq.gz	Fastqsanger.gz
	SRR2959434.fastq.gz	Fastqsanger.gz

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Danio rerio

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

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Project description:Emergence of neural crest identity is a key early step in melanoma formation [ChIP-Seq]

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Emergence of neural crest identity is a key early step in melanoma formation [ChIP-Seq]

Project description:The “cancerized field” concept posits that cells of a given tissue share a potentially oncogenic mutation or insult and are thus cancer-prone, yet only discreet clones within the field initiate tumor formation. In melanoma, tumors frequently (~50%) carry the oncogenic BRAFV600E mutation that is also nearly always present in benign nevi that rarely become melanoma. The zebrafish crestin gene is expressed embryonically in neural crest progenitors and is then specifically re-expressed in melanoma tumors. Here, we show by live imaging transgenic zebrafish crestin reporters that single melanocytes in a cancerized field with oncogenic BRAFV600E and p53 tumor suppressor loss undergo a change that recapitulates the neural crest progenitor (NCP) state, and patches of these cells initiate early melanoma. The crestin element is regulated by the NCP transcription factor sox10. Forced sox10 overexpression in melanocytes accelerated melanoma formation, consistent with reprogramming to the NCP state and activation of super-enhancers that lead to melanoma. Our work highlights the importance of the reemergence of the NCP state as a barrier to melanoma initiation.

2016-06-08 | GSE61825 | GEO

Emergence of neural crest identity is a key early step in melanoma formation [Affymetrix]

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RNA helicase DDX21 mediates nucleotide stress responses

Project description:The stress of nucleotide pool reduction regulates transcription in neural crest and melanoma cells. To better understand the molecular response caused by nucleotide stress, we designed a chemical suppressor screen for leflunomide, an inhibitor of dihydroorate dehydrogenase. We found that alterations in the progesterone receptor (Pgr) activity suppressed the neural crest effects of leflunomide. To clarify the mechanism of action, we found that the RNA helicase protein, Ddx21, binds to Pgr, and loss of function of Ddx21 conferred resistance to nucleotide stress in zebrafish embryos. At the molecular level, nucleotide stress reduces DDX21 chromatin occupancy and thus, target gene expression. Together our results show that DDX21 is a transcriptional sensor and mediator of the nucleotide stress response.

2020-02-06 | PXD014433 | Pride

Danio rerio

Project description:Emergence of neural crest identity is a key early step in melanoma formation [Affymetrix]

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