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Amplified dosage of the NKX2-1 lineage transcription factor controls its oncogenic role in lung adenocarcinoma [ATAC-seq]

ABSTRACT: Amplified dosage of the NKX2-1 lineage transcription factor controls its oncogenic role in lung adenocarcinoma [ATAC-seq]

PROVIDER: PRJNA954852 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24149649_1.fastq.gz	Fastqsanger.gz
	SRR24149649_2.fastq.gz	Fastqsanger.gz
	SRR24149650_1.fastq.gz	Fastqsanger.gz
	SRR24149650_2.fastq.gz	Fastqsanger.gz
	SRR24149651_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Amplified dosage of the NKX2-1 lineage transcription factor controls its oncogenic role in lung adenocarcinoma

Project description:This SuperSeries is composed of the SubSeries listed below. Amplification-mediated oncogene overexpression is a critical and widespread driver event in cancer, yet our understanding of how amplification and dosage mediate oncogene regulation is limited. Here, we find that the most significant focal amplification event in lung adenocarcinoma (LUAD) targets a lineage “super-enhancer” near the NKX2-1 lineage transcription factor. The NKX2-1 super-enhancer is targeted by focal and co-amplification with NKX2-1 and controls NKX2-1 expression and regulation. We find that NKX2-1 directly controls enhancer accessibility to drive a lineage-addicted state in LUAD. We precisely map the effects of NKX2-1 dosage modulation upon both overexpression and knockdown and identify both linear and non-linear regulation by NKX2-1 dosage. We find that NKX2-1 is a widespread dependency in LUAD cell lines and that NKX2-1 confers persistence to EGFR inhibitors. Our data suggest a defining role for dosage in the oncogenic regulation of amplified NKX2-1 and that amplified NKX2-1 lineage addiction defines LUAD tumors.

2025-03-25 | GSE229542 | GEO

Amplified dosage of the NKX2-1 lineage transcription factor controls its oncogenic role in lung adenocarcinoma [RNA-seq]

Project description:Amplification-mediated oncogene overexpression is a critical and widespread driver event in cancer, yet our understanding of how amplification and dosage mediate oncogene regulation is limited. Here, we find that the most significant focal amplification event in lung adenocarcinoma (LUAD) targets a lineage “super-enhancer” near the NKX2-1 lineage transcription factor. The NKX2-1 super-enhancer is targeted by focal and co-amplification with NKX2-1 and controls NKX2-1 expression and regulation. We find that NKX2-1 directly controls enhancer accessibility to drive a lineage-addicted state in LUAD. We precisely map the effects of NKX2-1 dosage modulation upon both overexpression and knockdown and identify both linear and non-linear regulation by NKX2-1 dosage. We find that NKX2-1 is a widespread dependency in LUAD cell lines and that NKX2-1 confers persistence to EGFR inhibitors. Our data suggest a defining role for dosage in the oncogenic regulation of amplified NKX2-1 and that amplified NKX2-1 lineage addiction defines LUAD tumors.

2025-03-25 | GSE229541 | GEO

Amplified dosage of the NKX2-1 lineage transcription factor controls its oncogenic role in lung adenocarcinoma [ChIP-seq]

2025-03-25 | GSE229540 | GEO

Amplified dosage of the NKX2-1 lineage transcription factor controls its oncogenic role in lung adenocarcinoma [ATAC-seq]

2025-03-25 | GSE229539 | GEO

Amplified dosage of the NKX2-1 lineage transcription factor controls its oncogenic role in lung adenocarcinoma [Hi-C]

2025-03-25 | GSE292519 | GEO

Amplified dosage of the NKX2-1 lineage transcription factor controls its oncogenic role in lung adenocarcinoma

Project description:Amplified dosage of the NKX2-1 lineage transcription factor controls its oncogenic role in lung adenocarcinoma

| PRJNA954846 | ENA

Amplified dosage of the NKX2-1 lineage transcription factor controls its oncogenic role in lung adenocarcinoma [ChIP-seq]

Project description:Amplified dosage of the NKX2-1 lineage transcription factor controls its oncogenic role in lung adenocarcinoma [ChIP-seq]

| PRJNA954851 | ENA

Amplified dosage of the NKX2-1 lineage transcription factor controls its oncogenic role in lung adenocarcinoma [RNA-seq]

Project description:Amplified dosage of the NKX2-1 lineage transcription factor controls its oncogenic role in lung adenocarcinoma [RNA-seq]

| PRJNA954856 | ENA

Amplified dosage of the NKX2-1 lineage transcription factor controls its oncogenic role in lung adenocarcinoma [Hi-C]

Project description:Amplified dosage of the NKX2-1 lineage transcription factor controls its oncogenic role in lung adenocarcinoma [Hi-C]

| PRJNA1238912 | ENA

NKX2-1 occupancy in human lung adenocarcinoma cell lines

Project description:The NKX2-1 transcription factor, a regulator of normal lung development, is the most significantly amplified gene in human lung adenocarcinoma. To better understand how genomic alterations of NKX2-1 drive tumorigenesis, we generated an expression signature associated with NKX2-1 amplification in human lung adenocarcinoma, and analyzed DNA binding sites of NKX2-1 by genome-wide chromatin immunoprecipitation from NKX2-1-amplified human lung adenocarcinoma cell lines. Combining these expression and cistromic analyses identified LMO3, itself encoding a transcription regulator, as a candidate direct transcriptional target of NKX2-1, in addition to consensus binding motifs including a nuclear hormone receptor signature and a Forkhead box motif in NKX2-1-bound sequences. RNA interference analysis of NKX2-1-amplified cells compared to non-amplified cells demonstrated that LMO3 mediates cell proliferation downstream of NKX2-1; cistromic analysis that NKX2-1 may cooperate with FOXA1. Our findings provide new insight into the transcriptional regulatory network of NKX2-1 and suggest that LMO3 is a transducer of lineage specific cell survival of NKX2-1-amplified lung adenocarcinomas.

2013-01-22 | GSE39998 | GEO

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