Comparison of CRISPR-Cas9 genome-edited JEG-3 YAP knockout and wild type choriocarcinoma cells.
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA601913 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10907700.fastq.gz | Fastqsanger.gz | |||
| SRR10907701.fastq.gz | Fastqsanger.gz | |||
| SRR10907702.fastq.gz | Fastqsanger.gz | |||
| SRR10907703.fastq.gz | Fastqsanger.gz | |||
| SRR10907704.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 48 |
Similar Datasets
Project description:The Hippo signalling-dependent co-activator YAP controls organ size by regulating cell proliferation, apoptosis, stem cell renewal and is involved in cell contact inhibition. Aim of this study was to identify human trophoblast-specific YAP regulated gene signatures by comparing YAP wilde type and YAP knock out JEG-3 coriocarcinoma cell lines. YAP knockout cell lines were established by CRISPR-Cas9 technology.
2020-05-19 | GSE143859 | GEO
Project description:The transcriptional co-activator TAZ/WWTR1 plays a central role in the Hippo signaling pathway and acts as crucial mediator in maintaining organ size and tissue homeostasis. Changes in its activity can lead to diseases, including cancer, due to uncontrolled cell growth or aberrant cellular behavior. The aim of this study was to identify gene signatures that are specifically regulated by TAZ in human trophoblast cells. This was achieved by comparing JEG-3 wild-type and TAZ knockout choriocarcinoma cells, generated with CRISPR-Cas9 technology.
2025-03-28 | GSE282831 | GEO
Project description:Comparison of CRISPR-Cas9 genome-edited JEG-3 TAZ/WWTR1 knockout and wild type choriocarcinoma cells
| PRJNA1190490 | ENA
Project description:Choriocarcinoma is one of the rare gynecological malignancies with aggressive behavior. Vorinostat is an approved HDAC inhibitor, and HDACs play important roles in regulating gene expression and modulating various cellular processes. Here, the human choriocarcinoma cell lines (JAR and JEG-3) were treated with 1 μM vorinostat or DMSO for 48 h. Then, total RNA was extracted, and transcriptome analysis was performed.
2021-12-25 | GSE192446 | GEO
Project description:We report the application of transcriptome sequencing for investigating of the hsa-miR-371a-5p and hsa-miR-518a-3p regulated genes. JAR, JEG-3 and BeWo choriocarcinoma cells were transfected with hsa-miR-371a-5p or hsa-miR-518a-3p inhibitors or control inhibitors. Totally, 237, 132 and 277 genes with > 2 folds change and adjusted P < 0.05 were upregulated in JAR, JEG-3 and BeWo cells respectively after hsa-miR-371a-5p knockdown. Meanwhile, 229, 269 and 191 genes were upregulated in JAR, JEG-3 and BeWo cells respectively after hsa-miR-518a-3p knockdown. The top upregulated genes included many oncogenes or oncogenesis associated ones. Enrichment analysis showed hsa-miR-371a-5p and hsa-miR-518a-3p regulated diverse pathways related to tumorigenesis and metastasis. Our results would be helpful for the searching of early molecular biomarkers and therapeutic targets for gestational trophoblastic neoplasia.
2018-11-01 | GSE106394 | GEO
Project description:We report a preliminary RNA-Seq data of MCF-7 cells edited in the FASN locus using CRISPR/Cas9. MCF-7 cells were edited by CRISPR/Cas9, screened by Surveyor assay, purified by limiting dilutions, validated by sanger sequencing, and characterized by diverse cellular analyses. Then, RNA from edited cells and non-edited controls were processed by TruSeq-RNA-Library-Prep-Kit and sequenced in a illumina equipment. Reads were aligned to hg38 in Galaxy using RNA-Star and transcripts were counted by FeatureCounts.
2019-12-25 | GSE142562 | GEO
Project description:Genome editing technologies have enabled the clinical development of allogeneic cellular therapies, yet the optimal gene editing modality for multiplex editing of therapeutic T cell product manufacturing remains elusive. In this study, we conducted a comprehensive comparison of CRISPR/Cas9 nuclease and adenine base editor (ABE) technologies in generating allogeneic chimeric antigen receptor (CAR) T cells, utilizing extensive in vitro and in vivo analyses. Both methods achieved high editing efficiencies across four target genes, critical for mitigating graft-versus-host disease and allograft rejection: TRAC or CD3E, B2M, CIITA, and PVR. Notably, ABE demonstrated higher manufacturing yields and distinct off-target profiles compared to Cas9, with translocations observed exclusively in Cas9-edited products. Functionally, ABE-edited CAR T cells exhibited superior in vitro effector functions under continuous antigen stimulation, including enhanced proliferative capacity and increased surface CAR expression. Transcriptomic analysis revealed that ABE editing resulted in reduced activation of p53 and DNA damage response pathways at baseline, along with sustained activation of metabolic pathways during antigen stress. Consistently, ATAC-seq data indicated that Cas9-edited, but not ABE-edited, CAR T cells showed enrichment of chromatin accessibility peaks associated with double-strand break repair and DNA damage response pathways. In a preclinical leukemia model, ABE-edited CAR T cells demonstrated improved tumor control and extended overall survival compared to their Cas9-edited counterparts. Collectively, these findings position ABE as a superior choice of Cas9 nucleases for multiplex gene editing in therapeutic T cells.
2025-04-09 | GSE290620 | GEO
Project description:Genome editing technologies have enabled the clinical development of allogeneic cellular therapies, yet the optimal gene editing modality for multiplex editing of therapeutic T cell product manufacturing remains elusive. In this study, we conducted a comprehensive comparison of CRISPR/Cas9 nuclease and adenine base editor (ABE) technologies in generating allogeneic chimeric antigen receptor (CAR) T cells, utilizing extensive in vitro and in vivo analyses. Both methods achieved high editing efficiencies across four target genes, critical for mitigating graft-versus-host disease and allograft rejection: TRAC or CD3E, B2M, CIITA, and PVR. Notably, ABE demonstrated higher manufacturing yields and distinct off-target profiles compared to Cas9, with translocations observed exclusively in Cas9-edited products. Functionally, ABE-edited CAR T cells exhibited superior in vitro effector functions under continuous antigen stimulation, including enhanced proliferative capacity and increased surface CAR expression. Transcriptomic analysis revealed that ABE editing resulted in reduced activation of p53 and DNA damage response pathways at baseline, along with sustained activation of metabolic pathways during antigen stress. Consistently, ATAC-seq data indicated that Cas9-edited, but not ABE-edited, CAR T cells showed enrichment of chromatin accessibility peaks associated with double-strand break repair and DNA damage response pathways. In a preclinical leukemia model, ABE-edited CAR T cells demonstrated improved tumor control and extended overall survival compared to their Cas9-edited counterparts. Collectively, these findings position ABE as a superior choice of Cas9 nucleases for multiplex gene editing in therapeutic T cells.
2025-04-09 | GSE290621 | GEO
Project description:Mouse embryonic stem cells (i.e., mESCs; line ESC 129-B13) were genetically modified using CRISPR-Cas9 to mutate the H3f3b locus, in order to carry homozygous lysine-to-alanine substitution of residues K9, K27 or K79. Two control mESC lines carrying knock-out of the H3f3a gene were used as background for the editing. Low-coverage whole-genome sequencing (~0.8/0.9X) was performed to assess the chromosomal integrity of the edited lines. Genomic DNA was extracted from each mutant and control mESC line and sonicated to obtain fragments of ~150-200bp on average. Fragmented DNA (~0.5-1 ug) was used for library preparation using the NEBNext Ultra II DNA library preparation kit (New England Biolabs). Sequencing was performed on a NextSeq500 platform in single-end mode (75bp reads).
2024-09-04 | E-MTAB-12867 | biostudies-arrayexpress
Project description:Gestational choriocarcinoma arises from the cells of conception and is usually characterized as a fast growing, invasive and aggressive malignancy. The overall incidence is approximately 1 case per 50,000 pregnancies and aside from increasing maternal age does not appear to have any other risk factors. In contrast to most malignancies, gestational choriocarcinoma is frequently treated on a clinical diagnosis without a biopsy and therefore tumor samples of sufficient quantity to permit detailed genetic analysis are exceptionally rare. As a result, no previous whole genome sequencing or methylation studies have been reported for this rare diagnosis. With the aim of investigating the potential contribution of epigenetic changes to the pathogenesis of this rare malignancy, we have performed a methylation analysis from routine processed FFPE material in a case of intra-placental choriocarcinoma.
2019-08-21 | GSE125386 | GEO