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Fascin actin-bundling protein 1 regulates non-small cell lung cancer progression by influencing transcription and splicing of tumorigenesis-related genes [IRIP-seq]

ABSTRACT: Fascin actin-bundling protein 1 regulates non-small cell lung cancer progression by influencing transcription and splicing of tumorigenesis-related genes [IRIP-seq]

PROVIDER: PRJNA983357 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24911862_1.fastq.gz	Fastqsanger.gz
	SRR24911862_2.fastq.gz	Fastqsanger.gz
	SRR24911863_1.fastq.gz	Fastqsanger.gz
	SRR24911863_2.fastq.gz	Fastqsanger.gz
	SRR24911864_1.fastq.gz	Fastqsanger.gz

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Fascin actin-bundling protein 1 regulates non-small cell lung cancer progression by influencing transcription and splicing of tumorigenesis-related genes

Project description:Fascin actin-bundling protein 1 regulates non-small cell lung cancer progression by influencing transcription and splicing of tumorigenesis-related genes

| PRJNA983342 | ENA

A Nanobody inhibitor of Fascin-1 actin-bundling activity and filopodia formation

Project description:Fascin-1 mediated actin-bundling activity is central to the generation of plasma membrane protrusions required for cell migration. Dysregulation of cellular protrusions is observed in metastatic cancers, where they are required for increased invasiveness, and this is often correlated with overexpression of Fascin-1. Therefore, there is interest in generating therapeutic Fascin-1 inhibitors. We present the identification of Nb 3E11, a nanobody inhibitor of Fascin-1 actin-bundling activity, filopodia formation and cell migration. The crystal structure of the Fascin-1/Nb 3E11 complex reveals the structural mechanism of inhibition. Nb 3E11 occludes an actin-binding site on the third -trefoil domain of Fascin-1 that is currently untargeted by chemical inhibitors and induces a conformational change in the adjacent domains to stabilise Fascin-1 in an inhibitory state similar to that adopted in the presence of small molecule inhibitors. Nb 3E11 can be utilised as a tool inhibitor molecule to aid in the development of Fascin-1 targeted therapeutics.

2024-03-25 | PXD038713 | Pride

Fascin actin-bundling protein 1 regulates non-small cell lung cancer progression by influencing transcription and splicing of tumorigenesis-related genes [RNA-seq]

Project description:Fascin actin-bundling protein 1 regulates non-small cell lung cancer progression by influencing transcription and splicing of tumorigenesis-related genes [RNA-seq]

| PRJNA983358 | ENA

Fascin actin-bundling protein 1 regulates non-small cell lung cancer progression by influencing transcription and splicing of tumorigenesis-related genes [RNA-seq]

Project description:Background. High mortality rates are prevalent among patients with non-small cell lung cancer (NSCLC), and effective therapeutic targets are key prognostic factors. Fascin actin-bundling protein 1 (FSCN1) promotes NSCLC; however, its role as an RNA-binding protein in NSCLC remains unexplored. Therefore, we aimed to explore FSCN1 expression and function in A549 cells. Method. We screened for alternative-splicing events and differentially expressed genes (DEGs) after FSCN1 silence via RNA-sequencing (RNA-seq). FSCN1 immunoprecipitation followed by RNA-seq were used to identify target genes whose mRNA expression and pre-mRNA alternative-splicing levels might be influenced by FSCN1. Results. Silencing FSCN1 in A549 cells affected malignant phenotypes; it inhibited proliferation, migration, and invasion, and promoted apoptosis. RNA-seq analysis revealed 2851 DEGs and 3057 alternatively spliced genes. Gene ontology-based functional enrichment analysis showed that downregulated DEGs and alternatively splicing genes were enriched for the cell-cycle. FSCN1 promoted the alternative splicing of cell-cycle-related mRNAs involved in tumorigenesis (i.e., BCCIP, DLGAP5, PRC1, RECQL5, WTAP, and SGO1). Combined analysis of FSCN1 RNA-binding targets and RNA-seq data suggested that FSCN1 might affect ACTG1, KRT7, and PDE3A expression by affecting the pre-mRNA alternative-splicing levels of NME4, NCOR2, and EEF1D FSCN1 to long non-coding RNA transcripts (RNASNHG20, NEAT1, NSD2, and FTH1), which were highly abundant. Overall, extensive transcriptome analysis of gene alternative splicing and expression levels was performed in cells transfected with FSCN1 short-interfering RNA. Our data provide global insights into the regulatory mechanisms mediated by FSCN1 and its target genes in lung cancer.

2023-07-01 | GSE234859 | GEO

Fascin actin-bundling protein 1 regulates non-small cell lung cancer progression by influencing transcription and splicing of tumorigenesis-related genes [IRIP-seq]

2023-07-01 | GSE234858 | GEO

Transcription profiling of human dendritic cells from PLOSL patients show abnormalities in pathways of actin bundling and immune response

Project description:This study was aimed to identify pathways associated with loss-of-function of the DAP12/TREM2 receptor complex and thus gain insight into pathogenesis of PLOSL (polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy). Transcript profiles of PLOSL patients' DCs showed differential expression of genes involved in actin bundling and immune response, but also for the stability of myelin and bone remodeling. Experiment Overall Design: Transcript profiles of in vitro differentiated DCs of three controls and five PLOSL patients were analyzed.

2008-11-06 | E-GEOD-3624 | biostudies-arrayexpress

Transcript profiles of DCs of PLOSL patients show abnormalities in pathways of actin bundling and immune response

Project description:This study was aimed to identify pathways associated with loss-of-function of the DAP12/TREM2 receptor complex and thus gain insight into pathogenesis of PLOSL (polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy). Transcript profiles of PLOSL patients' DCs showed differential expression of genes involved in actin bundling and immune response, but also for the stability of myelin and bone remodeling. Keywords: PLOSL patient samples vs. control samples

2007-06-01 | GSE3624 | GEO

A non-canonical function of tyrosyl-tRNA synthetase in actin bundling

Project description:Aminoacyl-tRNA synthetases are the largest protein family implicated in Charcot-Marie-Tooth disease (CMT), the most common inherited peripheral neuropathy that is currently incurable. These essential enzymes catalyze the attachment of amino acids to their cognate tRNAs, thereby enabling the protein biosynthesis in every cell. Surprisingly, loss of aminoacylation is not a prerequisite for CMT to occur, suggesting a disease mechanism associated with a gain of neurotoxic function. Via an unbiased genetic modifier screen in a Drosophila model of tyrosyl-tRNA synthetase (YARS) -induced CMT, we established a link between the tRNA-ligase and regulators of actin cytoskeleton. By investigating the interactome of YARS in cellulo we found this synthetase to be enriched in protein complexes containing actin and actin-modifying proteins. Follow up in vitro and in vivo studies demonstrated that YARS itself has not only actin binding- but also actin-bundling properties independent of its aminoacylation function. These non-canonical activities are evolutionary conserved and contribute to the organization of actin cytoskeleton in Drosophila neurons and in patient-derived cells. An enzymatically active YARSCMT mutant caused stronger actin bundling in vitro, disorganization of actin bundle-rich stress fibers in patient-derived cells and impaired multiple actin-based steps of the synaptic vesicle cycle in fly neurons. Genetic modulation of the F-actin organization state restored synaptic vesicle mobility and rescued hallmark electrophysiological and morphological features in the neurons of fruit flies expressing different YARSCMT mutations. Thus, we uncover a role of tyrosyl-tRNA synthetase in actin organization that is implicated in the CMT neuropathy.

2023-01-09 | PXD037630 | Pride

Ubiquitin-dependent remodeling of the actin cytoskeleton drives cell fusion

Project description:Cell-cell fusion is a frequent and essential event during development, and its dysregulation causes diseases ranging from infertility to muscle weakness. Fusing cells repeatedly need to remodel their plasma membrane by orchestrated formation and disassembly of cortical actin filaments, but how the dynamic reorganization of the actin cytoskeleton control is still poorly understood. Here, we identified a ubiquitin- dependent toggle switch that establishes reversible actin bundling during mammalian cell fusion. We found that EPS8-IRSp53 complexes stabilize cortical actin bundles at sites of cell contact, which in part pushes cells towards each other. Conversely, EPS8 monoubiquitylation by CUL3KCTD10 displaces EPS8-IRSp53 from membranes and counteracts actin bundling, a dual activity that allows apposed cells to progress with fusion. We conclude that cytoskeletal rearrangements during development are precisely controlled by ubiquitylation, raising the possibility to modulate the efficiency of cell-cell fusion for therapeutic benefit.

2020-12-22 | GSE161681 | GEO

Effect of FSCN1 gene inactivation in the H295R cell line

Project description:The actin-bundling protein fascin (FSCN1) is overexpressed in aggressive adrenocortical carcinoma (ACC) and represents a reliable prognostic indicator. We investigated the effects of FSCN1 inactivation by CRISPR/Cas9 in ACC H295R cells on global gene expression profiles in those cells. We performed gene expression profiling analysis using data obtained from RNA-seq of 2 different H295R control clones and 2 different FSCN1 KO clones (2 biological replicates for each clone).

2022-10-25 | GSE216008 | GEO