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

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

ORGANISM(S): Mus musculus

PROVIDER: GSE81257 | GEO | 2016/05/10

SECONDARY ACCESSION(S): PRJNA321071

REPOSITORIES: GEO

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

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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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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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Project description:We identified NFIB as a CARM1 substrate and showed that this transcription factor utilizes CARM1 as a coactivator. Importantly, NFIB harbors both oncogenic and metastatic activities, and is often overexpressed in small cell lung cancer (SCLC). Using a SCLC mouse model, we show that both CARM1 and the CARM1 methylation site on NFIB are critical for the rapid onset of SCLC. By performing the high-throughput sequecing analysis, we found that CARM1-null and NFIB-R388K mutant mouse SCLC tumors share the ability to regulate chromatin accessbility and have similar gene expression pattern.

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