Ontology highlight
ABSTRACT:
PROVIDER: PRJNA659812 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:<p>Adrenocortical carcinoma (ACC) is a rare endocrine malignancy with a high risk of relapse and metastatisation. The actin-bundling protein fascin (FSCN1) is overexpressed in aggressive ACC and represents a reliable prognostic indicator. FSCN1 has been shown to synergize with the Rho/Rac GEF VAV2 in enhancing the invasion properties of ACC cancer cells. Based on those results, we investigated the effects of FSCN1 inactivation by CRISPR/Cas9 or pharmacological blockade on the invasive properties of ACC cells, both <em>in vitro</em> and in an <em>in vivo</em> metastatic ACC zebrafish model. Here we showed that FSCN1 is a transcriptional target for Beta-catenin in H295R ACC cells and that its inactivation resulted in defects in cell attachment and proliferation. Additionally, FSCN1 knock-out modulated the expression of genes involved in cytoskeleton dynamics and cell adhesion. When SF-1 dosage was upregulated in H95R cells, activating their invasive capacities, FSCN1 knock-out reduced the number of filopodia, lamellipodia/ruffles and focal adhesions, while decreasing cell invasion in Matrigel. Similar effects were produced by the FSCN1 inhibitor G2-044, which also diminished the invasion of ACC cell lines (CU-ACC2, JIL-2266, MUC-1) expressing lower levels of FSCN1 than H295R. In the zebrafish model, metastases formation was significantly reduced in FSCN1 knock-out cells and G2-044 significantly reduced the number of metastases formed by ACC cells. Our results indicate that FSCN1 represents a new druggable target for ACC and provide the rationale for future clinical trials with FSCN1 inhibitors in patients with ACC, possibly in combination with immunotherapy.</p>
2023-03-20 | MTBLS6402 | MetaboLights
Project description:Transcriptome of the panx1a-knock out zebrafish
| PRJNA612878 | ENA
Project description:The goal of this study was to identify functional variants that play a role in exfoliation syndrome (XFS) pathogenesis. We sequenced the entire LOXL1 locus in 50 South African XFS cases and 50 matched controls. The most strongly associated variants in this dataset were found in a ~7kb region spanning the LOXL1 exon 1/intron 1 boundary. DNase hypersensitivity analysis was used to demonstrate that this region, which lies upstream of the LOXL1 antisense RNA (LOXL1-AS1), contains regulatory activity. determining of chromatin structural changes in 3 cell types.
2015-07-22 | E-GEOD-66877 | biostudies-arrayexpress
Project description:The goal of this study was to identify functional variants that play a role in exfoliation syndrome (XFS) pathogenesis. We sequenced the entire LOXL1 locus in 50 South African XFS cases and 50 matched controls. The most strongly associated variants in this dataset were found in a ~7kb region spanning the LOXL1 exon 1/intron 1 boundary. DNase hypersensitivity analysis was used to demonstrate that this region, which lies upstream of the LOXL1 antisense RNA (LOXL1-AS1), contains regulatory activity.
2015-07-22 | GSE66877 | GEO
Project description:CRISPR/Cas9 knock-out of the vtg1 and vtg3 genes was performed in zebrafish separately. This project involves proteomics screening for validation of the absence of targeted proteins in vtg1 and vtg3 and their variants in knocked out female zebrafish in eggs and investigating possible changes within the corresponding proteomes as a results of the absence of these specific vitellogenins and their variants.
2021-09-09 | PXD021302 | Pride
Project description:CRISPR/Cas9 knock-out of the vtg1 and vtg3 genes was performed in zebrafish separately. This project involves proteomics screening for validation of the absence of targeted proteins in vtg1 and vtg3 and their variants in knocked out female zebrafish in eggs and investigating possible changes within the corresponding proteomes as a results of the absence of these specific vitellogenins and their variants.
2023-10-09 | PXD042791 | Pride
Project description:Capn3 is responsible for human disease LGMD2B, but the mechanism is largely unknown. We generated two capn3b-/- mutant zebrafish alleles and found that p53 is highly enriched in the hepatocyte nucleoli of capn3b knock-out fish. Although homozygous capn3b knock-out mutants are viable and fertile, they display shorter length and lateral curvature phenotype in adulthood, which is similar to the limb-girdle muscular dystrophy type 2A (LGMD2A) patients caused by capn3 mutation. Using RNA-seq analysis of adult liver, we identified differentially expressed genes in capn3b-/- mutants. Genes involved in innate immune response pathways were highly enriched in the mutants' livers. This study presents the connection between capn3 deficiency and immune defects and provides new insights into LGMD2B therapy.
2024-03-07 | GSE198711 | GEO
Project description:Transcriptome of single and double pannexin1-knock out zebrafish lines
| PRJNA753704 | ENA