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CircCDYL association with hnRNPL modulates CDYL isoform switching in Breast Cancer cells

ABSTRACT: CircCDYL association with hnRNPL modulates CDYL isoform switching in Breast Cancer cells

PROVIDER: PRJNA1252746 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR33214213_1.fastq.gz	Fastqsanger.gz
	SRR33214213_2.fastq.gz	Fastqsanger.gz
	SRR33214214_1.fastq.gz	Fastqsanger.gz
	SRR33214214_2.fastq.gz	Fastqsanger.gz
	SRR33214215_1.fastq.gz	Fastqsanger.gz

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CircCDYL association with hnRNPL modulates CDYL isoform switching in Breast Cancer cells

Project description:Circular RNAs (circRNAs) are covalently closed transcripts involved in the regulation of different cellular processes, and their dysregulation has been frequently observed in cancer. In this study, we investigated the role of circCDYL, a circRNA generated from the CDYL gene, in modulating alternative splicing (AS) and isoform switching in breast cancer cells. Analysis of circRNA profiles in breast cancer cells showed that circCDYL expression increased in estrogen receptor alpha (ERα)-downregulated cells, suggesting a potential link between circCDYL-mediated regulation and ERα signaling pathways. RNA-Sequencing analysis following circCDYL knock-down in MCF-7 cells revealed significant alterations in the splicing pattern, with over 2,900 splicing events significantly affected. Through RNA immunoprecipitation and RNA pull-down assays, we found evidence of an association between circCDYL and the splicing factor hnRNPL. To explore the consequences of this association, we performed AS and isoform switching analysis after circCDYL and hnRNPL silencing, revealing significant effects on AS and a weaker modulation of isoform switching events. Furthermore, we observed that circCDYL and hnRNPL modulated CDYL isoform expression, as confirmed by isoform-specific qRT-PCR analysis. Chromatin immunoprecipitation assays also indicated changes in chromatin marks at the CDYL locus upon knock-down of circCDYL and hnRNPL. These results suggested a possible association between circCDYL and hnRNPL, which contributed to the regulation of alternative splicing in breast cancer cells and may be involved in the modulation of isoform expression and chromatin dynamics of CDYL gene.

2025-04-18 | GSE295065 | GEO

CircCDYL Association With hnRNPL Modulates CDYL Isoform Switching in Breast Cancer Cells.

Project description: Not available

| S-EPMC12485669 | biostudies-literature

NTRAS hnRNPL RNA sequencing in HUVECs

Project description:In the current project with aim to unequivocally characterize a novel splicing-regulatory network that proves to be a central mediator of endothelial barrier function and vascular integrity. At the core of this network is the endothelial enriched lncRNA NTRAS (annotated as RP11-354k1.1) is shown to control alternative splicing decisions in HUVECs through interplaying with splicing factor hnRNPL. Specifically, in the project we show that NTRAS sequesters the splicing factor hnRNPL through a CA dinucleotide motif, to enhance TJP1 exon 20 usage, thereby TJP1α+ isoform. In turn disrupting TJP1α+ isoform expression impaired endothelial barrier function. Collectively, this splicing-regulatory network might prove fundamental in unlocking new interventions strategic to prevent or reverse vascular leakage.

2022-01-10 | E-MTAB-11311 | biostudies-arrayexpress

Transcriptomic Regulation Driven by TCF12 Isoform Switching

Project description:Transcriptomic Regulation Driven by TCF12 Isoform Switching

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Isoform Switching in Small Intestine Epithelial Differentiation

Project description:Isoform Switching in Small Intestine Epithelial Differentiation

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Isoform Switching in Small Intestine Epithelial Differentiation

Project description:To investigate the genome-wide isoform switching events in the small intestinal epithelium, we compared duodenal BMP 24h treated duodenal crypt organoids vs untreated duodenal crypt organoids.

2026-07-04 | GSE232589 | GEO

CDYL ChIP-Seq in mouse hippocampus

Project description:Here we report that the epigenetic factor Chromodomain Y-like (CDYL) protein is a critical regulator for the initiation and maintenance of activity-dependent intrinsic neuroplasticity. Genome-wide ChIP-sequencing analysis revealed that CDYL regulates multiple neuronal functional pathways including voltage-gated ion channels in mouse brains. We showed that CDYL binds to a regulatory element in the intron region of SCN8A and mainly recruits H3K27me3 activity for transcriptional repression of the gene. Injection of lentivirally-delivered CDYL shRNA to rat hippocampal neurons resulted in augmented Nav1.6-mediated sodium currents, lower neuronal threshold and increased seizure susceptibility, whereas transgenic mice over-expressing CDYL had higher neuronal threshold and were less prone to epileptogenesis. Finally, examination of human brain tissues revealed decreased expression of CDYL and increased expression of SCN8A in the temporal lobe epilepsy group. Together, our findings indicate CDYL is a critical player for experience-dependent gene regulation in controlling intrinsic excitability, which potentially contributes to learning and memory and CNS disorders involving change in activity such as epilepsy.

2017-06-25 | GSE96721 | GEO

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Project description:Global isoform switching in esophageal adenocarcinoma (EAC) has not been previously characterized. This form of alternative splicing has recently been recognized as highly prevalent in multiple other cancers. In this study, isoform switch analysis was performed using next generation sequencing of RNA isolated from patient tissues across a continuum of histopathologies, ranging from low risk Barrett’s esophagus (BE) to BE with dysplasia and EAC. Patients were stratified based on histopathology.

2022-08-17 | GSE193946 | GEO

ChIP-seq data of CDYL in mouse dorsal root ganglia

Project description:We report that the epigenetic factor CDYL is crucial for pain processing. CDYL downstreams in mouse dorsal root ganglia (DRG) are mostly associated with neurological functions, including chemical synaptic transmission, regulation of membrane potential and ion transport. CDYL facilitates H3K27me3 deposition at the Kcnb1 intron region thus silencing Kv2.1 transcription. Loss function of CDYL enhances total Kv and Kv2.1 current density in DRG and knockdown of Kv2.1 reverses the pain-related phenotypes of Cdyl deficiency mice.

2022-02-08 | GSE190751 | GEO

Isoform switching events in Barrett's Esophagus and esophageal adenocarcinoma

Project description:Isoform switching events in Barrett's Esophagus and esophageal adenocarcinoma

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