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

ORGANISM(S): Mus musculus

PROVIDER: GSE228333 | GEO | 2023/11/07

REPOSITORIES: GEO

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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.

2023-11-07 | GSE227669 | 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

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

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

2016-07-29 | GSE82005 | 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.

2016-05-10 | GSE81256 | GEO

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 [ATAC-seq]

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

2016-05-10 | GSE81255 | GEO

Hepatocyte-specific knock-out of Nfib aggravates hepatocellular tumorigenesis via enhancing urea cycle

Project description:Purpose: Nuclear Factor I B (NFIB) has been reported to promote tumor growth, metastasis, and liver regeneration, but its mechanism in liver cancer is not fully elucidated. The present study aims to reveal the role of NFIB in hepatocellular carcinogenesis Methods:In our study, we constructed hepatocyte-specific NFIB gene knockout mice with CRISPR/Cas9 technology (Nfib-/-; Alb-cre), and induced liver cancer mouse model by intraperitoneal injection of DEN/CCl4 Results: First, we found that Nfib-/-; Alb-cre mice developed more tumor nodules and had heavier livers than wild-type mice. H&E staining indicated that the liver histological severity of Nfib-/- group was more serious than that of WT group. Then we found that the differentially expressed genes in the tumor tissue between Nfib-/- mice and wild type mice were enriched in urea cycle. Furthermore, ASS1 and CPS1, the core enzymes of the urea cycle, were significantly upregulated in Nfib-/- tumors. Subsequently, we validated that the expression of ASS1 and CPS1 increased after knockdown of NFIB by lentivirus in normal hepatocytes and also promoted cell proliferation in vitro. In addition, ChIP assay confirmed that NFIB can bind with promoter region of both ASS1 and CPS1 gene Conclusions:Our study reveals for the first time that hepatocyte-specific knock-out of Nfib aggravates hepatocellular tumor development by enhancing the urea cycle.

2022-06-23 | GSE200708 | 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

Distinct Function for ASCL1 and NEUROD1 in Pulmonary Neuroendocrine Tumors (RNA-seq)

Project description:Small cell lung carcinoma (SCLC) and large cell neuroendocrine carcinoma (LCNEC) are high-grade pulmonary neuroendocrine tumors. The neural basic helix-loop-helix (bHLH) transcription factors ASCL1 and NEUROD1 have been shown to play crucial roles in promoting the malignant behavior and survival of human SCLC cell lines. In this study, we find ASCL1 and NEUROD1 identify distinct neuroendocrine tumors, bind distinct genomic loci, and regulate mostly distinct genes. ASCL1 and NEUROD1 are often bound in super-enhancers that are associated with highly expressed genes in their respective SCLC cell lines suggesting different cell lineage of origin for these tumors. ASCL1 targets oncogenic genes such as MYCL1, RET, and NFIB, while NEUROD1 targets the oncogenic gene MYC. Although ASCL1 and NEUROD1 regulate different genes, many of these gene targets commonly contribute to neuroendocrine and cell migration function. ASCL1 in particular also regulates genes in the NOTCH pathway and genes important in cell-cycle dynamics. Finally, we demonstrate ASCL1 but not NEUROD1 is required for SCLC and LCNEC tumor formation in current in vivo genetic mouse models of pulmonary neuroendocrine tumors RNA-seq analysis performed on two ASCL1high and two NEUROD1high human SCLC cell lines to identify gene expression patterns in these cells. Also, we performed RNA-seq in mouse neuroendocrine lung tumors obtained from Trp53;Rb1;Rbl2 triple knockout model mice treated with Adeno-CMVCRE intratracheally.

2016-07-21 | E-GEOD-69393 | biostudies-arrayexpress

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