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GATA6 gene regulatory network drives multi drug resistance in cutaneous melanoma

ABSTRACT: GATA6 gene regulatory network drives multi drug resistance in cutaneous melanoma

PROVIDER: PRJNA690702 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13386575.fastq.gz	Fastqsanger.gz
	SRR13386576.fastq.gz	Fastqsanger.gz
	SRR13386577.fastq.gz	Fastqsanger.gz
	SRR13386578.fastq.gz	Fastqsanger.gz

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GATA6 gene regulatory network drives multi drug resistance in cutaneous melanoma

Project description:Transcriptional co-acticvators inhibition is proving to be a powerful mean against cancer cells that shown a novel hallmarks named transcriptional addiction. This dependecy on co-activars activity lays on their presence in clusters of enhancer regulatory regions called Super-enhancers (SEs) that establish high level of expression of genes important for cancer phisiology such as oncogenes and master transcription factors of the cellular lineage of origin. Among these co-activators in SEs is the kinase CDK7 of the basal transcription factor TFIIH. Here, using a large panel of melanoma cell lines, we observed an overall dependency of melanoma cells in CDK7 activity by inhibiting its function through the drug THZ1. However, by chronically exposing melanoma cells to THZ1, they univocally become resistant, switching phenotype toward a mesenchymal-like state. By comparing the transcriptome of artificial resistant and untreated cells in culture, we observed upregulation of the transcription factor GATA6 which control indeed a small regulon that includes genes involved in multi-drug resistance (MDR).

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Gene expression signature of Gata6 positive epidermal cells.

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Project description:Transcriptome analysis has uncovered a series of long noncoding RNAs (lncRNAs) transcribed during cell differentiation. Here, we uncovered lncRNA GATA6-AS1 is a functional lncRNA in definitive endoderm (DE) differentiation. We found GATA6-AS1 positively regulated the expression of endoderm key factor GATA6, which was different from previous reports in other biological contexts. Further investigation showed GATA6-AS1 interacted with SMAD2/3 and recruited SMAD2/3 to the promoter region of the GATA6 gene locus. In addition, overexpression of GATA6 was able to rescue the defect of DE differentiation due to the absence of GATA6-AS1, suggesting GATA6 was the functional target of GATA6-AS1 during endoderm differentiation. Ultimately, our study uncovers GATA6-AS1 is necessary for DE and pancreas differentiation, and reveals the detailed regulation mechanism between GATA6-AS1 and DE differentiation.

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