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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE227669 | GEO | 2023/11/07

REPOSITORIES: GEO

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NFIB dependent and independent mechanisms of metastasis in small cell lung cancer [RNA-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 RNA-seq of 10 individual tumors dissected from mouse lungs and livers.

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

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

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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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.

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

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

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

| PRJNA946306 | ENA

Project description:SAGA and ATAC are two related transcriptional coactivator complexes, sharing the same histone acetyltransferase (HAT) subunit. The HAT activities of SAGA and ATAC are required for metazoan development but the precise role of the two complexes in RNA polymerase II transcription in mammals is less understood. To determine whether SAGA and ATAC have redundant or specific functions dependent on their HAT activities, we compared the effects of HAT inactivation in each complex with that of inactivation of either SAGA or ATAC core subunits in mouse embryonic stem cells (ESCs). We show that core subunits of SAGA or ATAC subunits are required for complex assembly, mouse ESC growth and self-renewal. Additionally, ATAC, but not SAGA subunits are required for ESC viability by regulating the transcription of translation-related genes. Surprisingly, depletion of specific or shared HAT module subunits caused a global decrease in histone H3K9 acetylation, but did not result in significant phenotypic or transcriptional defects. Thus, our results indicate that SAGA and ATAC are differentially required for viability and self-renewal of mouse ESCs by regulating transcription through different pathways, in a HAT-independent manner.

2021-08-11 | PXD027026 | Pride

Nuclear Factor I/B is an Oncogene in Small Cell Lung Cancer

Project description:Small cell lung cancer (SCLC) is an aggressive cancer often diagnosed only after it has metastasized to distant sites (Meuwissen and Berns 2005; Cooper and Spiro 2006). Despite the need to better understand this disease, SCLC remains poorly characterized at the molecular and genomic levels (Forgacs et al. 2001; Pleasance et al. 2010). Using a genetically-engineered mouse model of SCLC driven by conditional deletion of Trp53 and Rb1 in the lung (Jonkers et al. 2001; Vooijs et al. 2002; Meuwissen et al. 2003; Sage et al. 2003), we identified several frequent, high-magnitude focal DNA copy number alterations in SCLC. We uncovered amplification of a novel, oncogenic transcription factor, Nuclear Factor I/B (Nfib) in the mouse SCLC model and in human SCLC. Functional studies indicate that NFIB regulates cell viability and proliferation during transformation. Gene expression analysis of two replicates each of two independent mSCLC cell lines (3583T3 and 3151T4) stably expressing Nfib, Mycl1 or both Nfib and Mycl1

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