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Nfib promotes Metastasis through a Widespread Increase in Chromatin Accessibility [ChIP-seq]

ABSTRACT: We describe Nfib as an important regulator of chromatin accessibility in SCLC.

ORGANISM(S): Mus musculus

PROVIDER: GSE81256 | GEO | 2016/05/10

SECONDARY ACCESSION(S): PRJNA321072

REPOSITORIES: GEO

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Nfib promotes Metastasis through a Widespread Increase in Chromatin Accessibility [RNA-seq]

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Project description:We describe Nfib as an important regulator of chromatin accessibility in Small cell lung cancer (SCLC).

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Nfib Promotes Metastasis through a Widespread Increase in Chromatin Accessibility.

Project description:Metastases are the main cause of cancer deaths, but the mechanisms underlying metastatic progression remain poorly understood. We isolated pure populations of cancer cells from primary tumors and metastases from a genetically engineered mouse model of human small cell lung cancer (SCLC) to investigate the mechanisms that drive the metastatic spread of this lethal cancer. Genome-wide characterization of chromatin accessibility revealed the opening of large numbers of distal regulatory elements across the genome during metastatic progression. These changes correlate with copy number amplification of the Nfib locus, and differentially accessible sites were highly enriched for Nfib transcription factor binding sites. Nfib is necessary and sufficient to increase chromatin accessibility at a large subset of the intergenic regions. Nfib promotes pro-metastatic neuronal gene expression programs and drives the metastatic ability of SCLC cells. The identification of widespread chromatin changes during SCLC progression reveals an unexpected global reprogramming during metastatic progression.

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Nfib promotes Metastasis through a Widespread Increase in Chromatin Accessibility

Project description:Nfib promotes Metastasis through a Widespread Increase in Chromatin Accessibility

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Nfib promotes Metastasis through a Widespread Increase in Chromatin Accessibility

Project description:This SuperSeries is composed of the SubSeries listed below.

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Nfib promotes Metastasis through a Widespread Increase in Chromatin Accessibility [ATAC-seq]

Project description:Nfib promotes Metastasis through a Widespread Increase in Chromatin Accessibility [ATAC-seq]

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NFIB is a driver of SCLC initiation, progression and metastasis in mouse and marks metastatic disease in patients

Project description:Small Cell Lung Cancer (SCLC) is the most aggressive type of lung cancer with early metastatic dissemination and invariable development of resistant disease for which no effective treatment is available to date. Mouse models of SCLC based on inactivation of Rb1 and Trp53 developed earlier showed frequent amplifications of two transcription factor genes: Nfib and Mycl. Overexpression of Nfib but not Mycl in SCLC mouse results in an enhanced and altered metastatic profile, and appears to be associated with genomic instability. NFIB promotes tumor heterogeneity with the concomitant expansive growth of poorly differentiated, highly proliferative, and invasive tumor cell populations. Consistent with the mouse data, NFIB expression in high-grade human neuroendocrine carcinomas correlates with advanced stage III/IV disease warranting its further assessment as a potentially valuable progression marker in a clinical setting. Genomic DNA from mouse small cell lung tumor samples was analyzed by mate pair sequencing and low coverage sequencing. And RNA from Nfib overexpressing mouse small cell lung cancer cell lines was further analyzed for high quality RNA profiles using Illumina Hiseq2500. This series contains only RNA-seq data.

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NFIB dependent and independent mechanisms of metastasis in small cell lung cancer [ATAC-seq]

Project description:Molecular characterization of lung tumors and liver metastases from SCLC mouse models with and without Nfib knockout. We performed gene expression profiling analysis using data obtained from ATAC-seq of 7 mouse SCLC cell lines.

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The NFIB/CARM1 Axis is a Therapeutic Target for Small Cell Lung Cancer

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2022-02-07 | GSE195843 | GEO

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