Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE303110 | GEO | 2025/09/11

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

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.

2025-09-11 | GSE303269 | GEO

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

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

| PRJNA1294186 | ENA

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.

2015-10-21 | GSE74188 | GEO

Capicua-dependent transcriptional changes in human cancer cell lines treated with trametinib

Project description:We performed a genome-scale CRISPR screen in a KRAS-mutant pancreatic cancer cell line treated with the MEK inhibitor trametinib, and found that loss of the transcriptional repressor CIC confers resistance to MEK inhibition. We determined that CIC loss also confers resistance to MEK or BRAF inhibition in lung cancer, colorectal cancer, and melanoma cell lines with mutant RAS or BRAF. CIC is a transcriptional repressor that is phosphorylated and inhibited by the MAPK pathway. We hypothesized that inhibition of the MAPK pathway would lead to activation of CIC and repression of CIC target genes. Loss of CIC would therefore restore expression of these genes, conferring drug resistance. To identify the relevant CIC target genes that mediate trametinib resistace, we generated 4 Cas9-expressing cell lines from different lineages and with different RAS or RAF mutations, and generated control (gGFP) or CIC-knockout (gCIC) cell lines. We treated cells with DMSO or trametinib for 24 hours, and performed NRA-seq. We found that trametinib treatment reduces expression of at least one member of the PEA3 family of ETS transcription factors (ETV1, ETV4, and ETV5) in all cell lines assessed, and that loss of CIC results in maintained expression of these genes despite MEK inhibition. We further validated that ETV1, 4, and 5 expression was necessary for resistance mediated by CIC loss; and that ETV1, 4, or 5 expression was sufficient to confer trametinib resistance.

2017-05-31 | GSE78519 | GEO

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.

2024-01-31 | GSE248116 | GEO

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

2024-01-31 | GSE248040 | GEO

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

The RNA-Seq transcriptome of human prostate cancer cell line depleted of CIC

Project description:To identify which genes were regulated by CIC in human prostate cancer cell, the effect of CIC knockdown on PC3 cell transcriptome was determined

2015-12-31 | GSE64025 | GEO

RNAseq to compare chemokine expression profiles in KP line vs total KP lung tumors tissues

Project description:To investigate the chemokines expressed by the KP cancer line and to compare it to chemokines expressed in lung tissues upon inoculation of KP tumor cells

2022-04-07 | GSE200126 | GEO

Project description:kp Metagenome

| PRJNA561246 | ENA