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Characterization of CIC binding to chromatin in murine KP and KPCic cell lines

ABSTRACT: Characterization of CIC binding to chromatin in murine KP and KPCic cell lines

PROVIDER: PRJNA1294186 | ENA |

REPOSITORIES: ENA

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Characterization of CIC binding to chromatin in murine KP and KPCic cell lines

Project description:CIC binding was determined in KP murine lung cancer cells in untreated cells as well as after treatment with trametinib to enhance CIC binding to DNA. As a negative control, CIC binding was also determined in KPCic cells that express a non-functional CIC incapable of DNA binding.

2025-09-11 | GSE303110 | GEO

Transcriptomic analysis of lung adenocarcinomas from KP and KPCic mice

Project description:The transcriptional repressor Capicua (CIC) is negatively regulated by KRAS/MAPK signaling. To characterize the impact of CIC loss on KrasG12V/Trp53-KO-driven lung adenocarcinomas in mice, the transcriptome of tumors from Kras (+/LSLG12V); Trp53 (lox/lox) [KP] and Kras (+/LSLG12V); Trp53 (lox/lox); Cic (lox/lox) [KPCic] mice are compared.

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Genome-wide maps of Cic binding sites in intestinal stem cells (ISCs) & Entroblasts (EBs) and transcriptome profiling of Cic depleted progenitor cells (ISCs & Ebs).

Project description:Purpose: Cic is a transcription factor regulating intestinal stem cell (ISC) proliferation as downstream effector of EGFR signaling pathway. ISC-specific mRNA expression profiling and DNA binding mapping using DamID were performed to identify potential target of Cic. Methods: Total RNA was isolated from GFP+ FACS sorted cells and sent for sequencing after amplification. Conclusions: We identified potential target genes of Cic, which is differetially expressed in Cic depleted ISCs and also associated Cic binding peaks.

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Expression data from KP and KPY murine sarcoma tumors

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RNA-Seq Analysis of mouse lung cancer cell lines derived from KP mice and Reprogrammed somatic cells

Project description:We report the gene expression profile of three murine lung cancer cell lines, and also comparing the similarities of gene expression between KP mice-derived tumor cells and Regrogrammed somatic cells-derived tumor cells.

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Expression data from CIC wild type and knockout cell lines

Project description:Type I low-grade gliomas (LGGs), characterized by 1p/19q co-deletions and IDH1/2 mutations, show superior overall survival compared to other gliomas. Approximately 70% of cases harbour mutations in the Capicua (CIC) gene, whose product is a transcriptional repressor whose transcriptional network has yet to be extensively studied in human cells. To address this, we developed CIC knockout cell lines and used transcriptome analyses to study the consequences of CIC loss. Results were further compared to data for Type I LGGs and stomach adenocarcinomas from The Cancer Genome Atlas (TCGA). We find that CIC appears to regulate the expression of genes involved in cell-cell adhesion and nervous system development. CIC deficiency is also found to be associated with a MEK activation transcriptional signature and to act as an effector of MEK signalling. Loss of CIC may thus present a novel mechanism for the dysregulation of this and other oncogenic pathways.

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CIC-DUX4 chromatin profiling reveals new epigenetic dependencies and actionable therpaeutic targets in CIC-rearranged sarcomas [RNA-seq]

Project description:CIC-DUX4-rearranged sarcoma (CDS) is a rare and aggressive soft tissue tumor that occurs most frequently in young adults. The key oncogenic driver of this disease is the expression of the CIC-DUX4 fusion protein as a result of chromosomal rearrangements. CIC-DUX4 displays chromatin binding properties, and is therefore believed to function as an aberrant transcription factor. However, the chromatin remodeling events induced by CIC-DUX4 are not well understood, limiting our ability to identify new mechanism-based therapeutic strategies for these patients. Here we generated a genome wide profile of CIC-DUX4 DNA occupancy and associated chromatin states in human CDS cell models and primary tumors. Combining chromatin profiling, proximity ligation assays, as well as genetic and pharmacological perturbations, we show that CIC-DUX4 operates as a potent transcriptional activator at its binding sites. This property is in contrast with the repressive function of the wild type CIC protein, and is mainly mediated through the direct interaction of CIC-DUX4 with the acetyltransferase p300. In keeping with this, we show p300 to be essential for CDS tumor cell proliferation, and its pharmacological inhibition to significantly impact tumor growth in vitro andin vivo. Taken together, our study elucidates the mechanisms underpinning CIC-DUX4-mediated transcriptional regulation and suggests a potential therapeutic approach for the clinical management of CDS patients.

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CIC-DUX4 chromatin profiling reveals new epigenetic dependencies and actionable therpaeutic targets in CIC-rearranged sarcomas [ChIP-seq]

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RNA-seq of Glioma Neural Stem (GNS) cell line G144 after MEK inhibition in wild type (WT) and CIC (Capicua) depleted cells.

Project description:We identified genome-wide binding patterns of CIC in several different cell types and find that CIC target genes are enriched for MAPK effector genes involved in cell cycle regulation and proliferation. CIC binding to its target genes is abolished by high MAPK activity, which leads to hyperacetylation and their transcriptional activation. Inhibition of MAPK signaling via MEK inhibition leads to recruitment of CIC to its target genes. ChIP-seq data of G144 cells after MEK inhibition and CIC knockout is available under accession E-MTAB-6682

2018-05-31 | E-MTAB-6681 | biostudies-arrayexpress

Expression data from KP and KPY murine sarcoma tumors

Project description:Expression data from KP and KPY murine sarcoma tumors

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