Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

GRHL3 activates FSCN1 to relax cell adhesions between migrating keratinocytes in the wound front

ABSTRACT: GRHL3 activates FSCN1 to relax cell adhesions between migrating keratinocytes in the wound front

PROVIDER: PRJNA722266 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR14244165.fastq.gz	Fastqsanger.gz
	SRR14244166.fastq.gz	Fastqsanger.gz
	SRR14244167.fastq.gz	Fastqsanger.gz
	SRR14244168.fastq.gz	Fastqsanger.gz
	SRR14244169.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 15

Similar Datasets

GRHL3 activates FSCN1 to relax cell adhesions between migrating keratinocytes in the wound front

Project description:identify an underlying mechanism a new pathway where GRHL3 activates the Fscn1 gene to effect cell-cell loosening in the migrating wound front

2021-10-13 | GSE172161 | GEO

GRHL3 activates FSCN1 to relax cell-cell adhesions between migrating keratinocytes during wound reepithelialization.

Project description:The migrating keratinocyte wound front is required for skin wound closure. Despite significant advances in wound healing research, we do not fully understand the molecular mechanisms that orchestrate collective keratinocyte migration. Here, we show that, in the wound front, the epidermal transcription factor Grainyhead like-3 (GRHL3) mediates decreased expression of the adherens junction protein E-cadherin; this results in relaxed adhesions between suprabasal keratinocytes, thus promoting collective cell migration and wound closure. Wound fronts from mice lacking GRHL3 in epithelial cells (Grhl3-cKO) have lower expression of Fascin-1 (FSCN1), a known negative regulator of E-cadherin. Assay for Transposase-Accessible Chromatin using sequencing (ATAC-seq) on wounded keratinocytes shows decreased wound-induced chromatin accessibility near the Fscn1 gene in Grhl3-cKO mice, a region enriched for GRHL3 motifs. These data reveal a wound-induced GRHL3/FSCN1/E-cadherin pathway that regulates keratinocyte-keratinocyte adhesion during wound-front migration; this pathway is activated in acute human wounds and is altered in diabetic wounds in mice, suggesting translational relevance.

| S-EPMC8492311 | biostudies-literature

the RNA binding property of FSCN1

Project description:To investigate the RNA binding property of FSCN1 in ESCC, RNA immunoprecipitation (RIP) was performed using an FSCN1 monoclonal antibody in ECA-109 cell lysate

2022-03-05 | GSE197621 | GEO

Proteomic Analysis of FSCN1-Interacting Proteins in LSCC cells

Project description:Fascin actin-bundling protein 1 (FSCN1) is an evolutionarily conserved actin-bundling protein that plays a critical role in cell migration, motility, adhesion and cellular interactions. Although multiple clinical studies have implicated the expression of FSCN1 in laryngeal squamous cell carcinoma (LSCC) progression, the precise mechanism of FSCN1 in the process has not been clearly elucidated. To define FSCN1 function, we characterized FSCN1-interacting proteins in LSCC cells by immunoprecipitation followed by LC-MS/MS. After data filtering, 119 proteins with expression in both the Hep-2 and TU-177 cell samples were identified as FSCN1-interacting partners. With in-depth bioinformatics analysis, we linked FSCN1 to critical cellular processes including cell adhesion, glycolysis/gluconeogenesis, regulation of protein ubiquitination, ribosomal RNA processing and small molecule metabolism. We discuss the interactions between FSCN1 and some of the newly validated partners. The identification of these potential partners of FSCN1 expands our knowledge of the FSCN1 interactome and provides a valuable resource for understanding the functions of this protein in LSCC progression.

2019-09-09 | PXD013072 | Pride

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

FSCN1 promotes esophageal carcinoma progression through downregulating PTK6 via its RNA-binding protein effect

Project description:To explore the downstream molecules of FSCN1, shRNA targeting FSCN1 was designed and transfected into the ESCC cell line, ECA-109. Whole-genome expression profiling was performed to screen for related molecules. To investigate the RNA binding property of FSCN1 in ESCC, RNA immunoprecipitation (RIP) was performed using an FSCN1 monoclonal antibody in ECA-109 cell lysate, and the associated RNA was analyzed by RNA-seq.

2022-03-05 | GSE197624 | GEO

Genome-wide analysis of gene expression regulated by FSCN1 in cervical cancer HeLa cells

Project description:FSCN1 has been reported to be dysregulated in cervical cancers. However, the genome-wide regulated targets of FSCN1 is still unclear in cervical cancers. Here, the gene expression profile of HeLa cells transfected with FSCN1 shRNA (shFSCN1) were compared with cells transfected with empty vector (shCtrl). The results showed that shFSCN1 extensively affects the transcriptional level of 5, 043 genes in HeLa cells. There were more up-regulated genes (3, 870) than down-regulated ones (1, 173) after FSCN1 was knocked down in HeLa cells. GO analysis showed that the up-regulated genes were associated with transcription regulation and DNA binding. The down-regulated genes were enriched in some cancer associated pathway including angiogenesis and cell adhesion. In particular, FSCN1 positilvely regulated ANGPTL4 in HeLa cells. Compared to normal tissue, both FSCN1 and ANGPTL4 showed a higher expression in cervical tumor tissue. Moreover, ANGPTL4 was also positilvely correlated with expression of FSCN1 in cervical tumor tissue of TCGA. In conclusion, our study provide important cues for further study on the regulatory mechanism of FSCN1 in cervical cancer.

2022-01-20 | GSE149450 | GEO

JUN promotes abdominal adhesions in mice and humans

Project description:Adhesions are fibrotic scars that form between abdominal organs following surgery or infection, and may cause bowel obstruction, chronic pain, or infertility. Adhesions occur post-operatively in 50-90% of all open abdominal operations and as such, represent an enormous clinical problem impacting hundreds of millions of patients worldwide. Our understanding of the biology of adhesion formation is very limited, which explains why there are essentially no available treatments that prevent adhesions. In this study, we systemically analyzed abdominal adhesions in mouse and human tissues gene expression using bulk- and sc-RNA-seq technologies to characterize the fibroblasts responsible for this devastating pathology.

2020-07-08 | GSE153929 | GEO

Screening of differentially expressed genes in LSCC cells knocking down FSCN1

Project description:Laryngeal squamous cell carcinoma (LSCC) is a common malignant tumor with a poor prognosis. Fascin actin-bundling protein 1 (FSCN1) has been reported to play a crucial role in LSCC development and progression, but the underlying molecular mechanisms remain unknown. Here, a whole transcriptome microarray analysis was performed to screen for differentially expressed genes in FSCN1 knockdown cells. We identified 1063 differentially expressed mRNA transcripts. Functional annotation revealed that these differentially expressed genes (DEGs) were involved in multiple biological functions such as transcriptional regulation, response to radiation, focal adhesion, ECM-receptor interaction, steroid biosynthesis, and others. Through co-expression and protein-protein interaction analysis, we linked FSCN1 to novel functions, including defense response to virus and steroid biosynthesis.

2024-02-17 | GSE255143 | GEO

the RNA binding property of FSCN1

Project description:the RNA binding property of FSCN1

| PRJNA811187 | ENA