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Nfib promotes Metastasis through a Widespread Increase in Chromatin Accessibility

ABSTRACT: Nfib promotes Metastasis through a Widespread Increase in Chromatin Accessibility

PROVIDER: PRJNA321069 | ENA |

REPOSITORIES: ENA

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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]

| PRJNA321073 | ENA

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

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

2016-05-10 | GSE81257 | GEO

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

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

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

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: Not available

| S-EPMC5004630 | biostudies-literature

Nfib promotes Metastasis through a Widespread Increase in Chromatin Accessibility

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

2016-05-10 | GSE81258 | GEO

Mus musculus

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

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Mus musculus

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

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RNA-Seq of 3 breast cancer models to investigate NFIB signalling role in metastatic colonization.

Project description:Next Generation Sequencing was applied to investigate molecular mechanisms underlying the increased metastatic colonization driven by Nfib. Global transcriptional profiling of primary tumours derived from Nfib high-expression models (LM1 and LM9) and Nfib low-expression models (HR1) allowed to identify Ero1l as a mediator of metastasis upon Nfib upregulation.

2021-01-15 | GSE144392 | GEO

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.

2016-07-29 | E-GEOD-82005 | biostudies-arrayexpress

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