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Mus musculus strain:FVB/n 129/Ola

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

PROVIDER: PRJNA323577 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3603930.fastq.gz	Fastqsanger.gz
	SRR3605280.fastq.gz	Fastqsanger.gz
	SRR3605290.fastq.gz	Fastqsanger.gz
	SRR3605300_1.fastq.gz	Fastqsanger.gz
	SRR3605300_2.fastq.gz	Fastqsanger.gz

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Mus musculus

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

| PRJNA323605 | ENA

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

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.

2022-02-07 | GSE195843 | GEO

single-cell RNA-sequence data of clinical small cell lung cancer samples

Project description:Small cell lung cancer (SCLC) is known for its high metastatic potential, with most patients demonstrating clinically evident metastases in multiple organs at diagnosis. The factors contributing to this exceptional metastatic capacity have not been defined. To bridge this gap, we compared gene expression in SCLC patient samples who never experienced metastasis or relapse throughout their clinical course, versus primary SCLC patient samples from more typical patients who had metastatic disease at diagnosis. This analysis identified FOXA2 as a transcription factor strongly associated with SCLC metastasis. Subsequent analyses in experimental models demonstrated that FOXA2 induces a fetal neuroendocrine gene expression program and promotes multi-site metastasis. Moreover, we identified ASCL1, a transcription factor known for its initiating role in SCLC tumorigenesis, as a direct binder of the FOXA2 promoter and regulator of FOXA2 expression. Taken together, these data define the ASCL1-FOXA2 axis as a critical driver of multiorgan SCLC metastasis.

2025-04-13 | GSE281740 | GEO

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

2016-07-29 | GSE82005 | GEO

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

2011-12-08 | E-GEOD-29533 | biostudies-arrayexpress

RNA-Seq of 2 lung metastatic breast cancer cell lines and their Nfib Kos.

Project description:Next Generation Sequencing was applied to investigate molecular mechanisms underlying the increased metastatic colonization driven by Nfib. Global transcriptional profiling of the lung metastatic cell lines and respective KOs allowed to identify Ero1l as a mediator of metastasis upon Nfib upregulation.

2021-01-15 | GSE144393 | GEO

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

RNA-sequence data of clinically never-metastatic primary small cell lung cancer cases and small cell lung cancer metastasis cases, FOXA2 knock-down and overexpression in cell lines

2025-04-13 | GSE281525 | GEO

Therapeutic targeting ERRγ suppresses metastasis via extracellular matrix remodeling in small cell lung cancer (ChIP-Seq)

Project description:Small-cell lung cancer (SCLC) is the most aggressive and lethal type of lung cancer, characterized by limited treatment options, early and frequent metastasis. However, the determinants of metastasis in SCLC are poorly defined. Here, we show that estrogen-related receptor gamma (ERRγ) is overexpressed in metastatic SCLC tumors, and it is positively associated with SCLC progression. ERRγ functions as an essential activator of ECM remodeling and cell adhesion, two critical steps in metastasis, by directly regulating the expression of major genes involved in these processes. Genetic and pharmacological inhibition of ERRγ markedly reduces collagen production, cell-matrix adhesion, microfilaments production, and eventually blocks SCLC cell invasion and tumor metastasis. Notably, ERRγ antagonists significantly suppress tumor growth and metastasis and restore resistant SCLC vulnerability to chemotherapy in multiple cell-derived and patient-derived xenograft models. Taken together, these findings establish ERRγ as an attractive target for metastatic SCLC and provide a potential pharmacological strategy for treating this lethal disease.

2024-05-15 | GSE259272 | GEO

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