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NRF2-dependent transcriptome and H3K27ac distribution in non-small cell lung cancer

ABSTRACT: NRF2-dependent transcriptome and H3K27ac distribution in non-small cell lung cancer

PROVIDER: PRJNA486927 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7726220_1.fastq.gz	Fastqsanger.gz
	SRR7726220_2.fastq.gz	Fastqsanger.gz
	SRR7726230_1.fastq.gz	Fastqsanger.gz
	SRR7726230_2.fastq.gz	Fastqsanger.gz
	SRR7726240_1.fastq.gz	Fastqsanger.gz

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Project description:Nuclear factor erythroid 2-related factor 2 (NRF2) is a stress responsive transcription factor that is mutationally activated in a subset (~25%) of clinically-aggressive non-small cell lung cancers(NSCLC). Mechanistic insight into drivers of the NRF2 dependency remains poorly understood. Here, we defined a novel NRF2 target gene set linked to NRF2-dependency in cancer cell lines,and observed that a significant portion of these genes is devoid of promoter-proximal NRF2. Using integrated genomic analyses, we characterized extensive NRF2-dependent enhancer RNA (eRNA) synthesis and NRF2-mediated H3K27ac deposition at proximal and distal enhancer regions regulating these genes. While CBP/p300 is a well-validated direct interaction partner of NRF2 with prominent functions at enhancers, we report that this interaction is not required for NRF2-dependent NSCLC cell growth, indicating that NRF2 can sustain sufficient transcriptional activity in the absence of CBP/p300 coactivation. Broad metabolic profiling established a primary role for CBP/p300 in NRF2-dependent accumulation of glutathione and glutathione-related metabolites. While redox homeostasis via enhanced glutathione production is commonly associated with the normal physiological role of NRF2, collectively our results suggest that NRF2-dependent cancer cell growth does not require this enhanced glutathione production.

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