Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1094995 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR28521019_1.fastq.gz | Fastqsanger.gz | |||
| SRR28521019_2.fastq.gz | Fastqsanger.gz | |||
| SRR28521024_1.fastq.gz | Fastqsanger.gz | |||
| SRR28521024_2.fastq.gz | Fastqsanger.gz |
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Project description:Jurkat clone E6-1 is a human T-cell line derived from a paediatric case of acute leukaemia, and is frequently employed as a model T-cell for immunology research. In this study, we characterised genomic, transcriptomic, and functional features of Jurkat clone E6-1 cells stored in three different laboratories, and compared these to Jurkat E6-1 cells from the ATCC. Jurkat clone E6-1 populations were first karyotyped, which results showing marked cytogenomic heterogeneity between cell line. These results were confirmed through chromosomal microarray analysis. Whole exome sequencing was then conducted on each cell line, and revealed distinct mutational profiles between populations. Mutational differences between Jurkat clone E6-1 populations detected by cytogenomic approaches and whole exome sequencing led to divergent transcriptomic profiles identified by bulk RNA sequencing, which, in turn, impacted cellular phenotype and function shown by flow cytometry and multiplex cytokine bead array data. Overall, we found substantial genomic heterogeneity between and within Jurkat clone E6-1 cells, resulting in significant differences in gene expression and function. This research highlights the extreme genomic instability of Jurkat clone E6-1 cells, the importance of monitoring cell passage number and procuring fresh cell line stocks, and the value of multi-omic approaches to characterise cell lines to improve the accuracy, reproducibility, and translatability of research.
2025-04-08 | GSE263543 | GEO
Project description:Genomic instability of Jurkat clone E6-1 T-cell lines affect gene expression and function: implications for T-cell researchers
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Project description:HIV-1 virion production is inefficient in cells derived from mice and other rodents. Inefficient production maps, in part, to a species-specific polymorphism in the cellular gene, CCNT1. In human cells, the HIV-1 Tat protein hijacks the positive transcription elongation factor (p-TEFb) complex, composed of CCNT1 and the cellular kinase CDK9, to promote viral transcript elongation and thereby increasing net viral gene expression and virion production. In mouse cells, Tat-dependent viral transcription is poor, reflecting the inability of Tat to engage p-TEFb because of a species-specific tyrosine residue at position 261 in the mouse ortholog of CCNT1. Humans encode a cysteine at the equivalent position which Tat requires for efficient p-TEFb usage. Here, we used CRISPR/Cas9 genome engineering to substitute the native cysteine with the rodent-encoded tyrosine (C261Y) in the human Jurkat T cell line (E6-1 clone). We derived two independent Jurkat T cell clones with all endogenous CCNT1 encoding the C261Y substitution. In an effort to understand net impacts to cellular and viral gene expression, we compared the transcriptomes of uninfected parental Jurkat T cells (E6-1 clone) to the two derived clones (C1 and C2, CCNT1.C261Y).
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Project description:HOXA9 transcriptomic analysis in GBM cell lines (U87MG, U251 and primary GBML18) and in immortalized human astrocytes (hTERT/E6/E7)
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Project description:Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has been shown to be a potent inducer of apoptosis in various cancer cell lines and primary cancer cells. However, in clinical trials administration of recombinant TRAIL or TRAIL death receptor agonists did not show sufficient efficacy for treatment of tested malignant disorders compared to standard chemotherapy. Acquired resistance of cancer cells to TRAIL and to other “death receptor” ligands may explain not only the inability of TRAIL and TRAIL “death receptor” agonists to achieve the clearance of cancer cells in vivo but also the escape of cancer cells from immune cell – mediated killing. Selective pressure of TRAIL on TRAIL-sensitive Jurkat T-lymphoblastic leukemia cells provided several TRAIL resistant Jurkat cell line clones (TR1, TR2, TR3). We showed that acquired TRAIL resistance was associated with complex disruption of both extrinsic and intrinsic apoptotic pathways manifested by acquired multi-drug resistant phenotype of TR1, TR2, and TR3 clones. To identify changes associated with TRAIL resistance of Jurkat cells we performed genome-wide gene expression analysis of TRAIL-resistant clones (TR) and compared to WT Jurkat cells. We identified significantly increased expression (1.33-fold change with adjusted p < 0.05) of 73 genes in TR1 clone, 53 genes in TR2 clone and 8 genes in TR3 clone, and significant decrease in expression (0.75-fold change with adjusted p < 0.05) of 174 genes in TR1 clone, 36 genes in TR2 clone and 28 genes in TR3 clone. There was an overlap of only 2 significantly overexpressed (midkine / MDK and zinc finger and BTB domain containing 16 gene / ZBTB16 / PLZF) and 4 downregulated genes (YAP1, IGJ, EIF1AY, RPS4Y1) in all three TR clones.
2016-06-15 | GSE38743 | GEO
Project description:Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has been shown to be a potent inducer of apoptosis in various cancer cell lines and primary cancer cells. However, in clinical trials administration of recombinant TRAIL or TRAIL death receptor agonists did not show sufficient efficacy for treatment of tested malignant disorders compared to standard chemotherapy. Acquired resistance of cancer cells to TRAIL and to other âdeath receptorâ ligands may explain not only the inability of TRAIL and TRAIL âdeath receptorâ agonists to achieve the clearance of cancer cells in vivo but also the escape of cancer cells from immune cell â mediated killing. Selective pressure of TRAIL on TRAIL-sensitive Jurkat T-lymphoblastic leukemia cells provided several TRAIL resistant Jurkat cell line clones (TR1, TR2, TR3). We showed that acquired TRAIL resistance was associated with complex disruption of both extrinsic and intrinsic apoptotic pathways manifested by acquired multi-drug resistant phenotype of TR1, TR2, and TR3 clones. To identify changes associated with TRAIL resistance of Jurkat cells we performed genome-wide gene expression analysis of TRAIL-resistant clones (TR) and compared to WT Jurkat cells. We identified significantly increased expression (1.33-fold change with adjusted p < 0.05) of 73 genes in TR1 clone, 53 genes in TR2 clone and 8 genes in TR3 clone, and significant decrease in expression (0.75-fold change with adjusted p < 0.05) of 174 genes in TR1 clone, 36 genes in TR2 clone and 28 genes in TR3 clone. There was an overlap of only 2 significantly overexpressed (midkine / MDK and zinc finger and BTB domain containing 16 gene / ZBTB16 / PLZF) and 4 downregulated genes (YAP1, IGJ, EIF1AY, RPS4Y1) in all three TR clones. Total cellular RNA was isolated from biologic duplicates of untreated Jurkat cells (WT) and TRAIL resistant Jurkat cell line subclones (TR1, TR2, TR3) established by selective pressure of TRAIL 1000 ng/mL on Jurkat cells over the period of 12 weeks.
2016-06-15 | E-GEOD-38743 | biostudies-arrayexpress
Project description:Bulk RNA Sequencing of Jurkat E6-1 & JLat9.2 CD4+ T cells Treated with 100IU/mL IFNb
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Project description:FIP-fve, a fungal fruiting body protein from Flammulina velutipes, has potential immunomodulatory properties. Here, we investigated the immunomodulation mechanism of FIP-fve in Jurkat E6-1 cells by conducting cell viability assay and IL-2 release assay. Kinase inhibitors experiment and proteomics analysis were also involved in the mechanism study. It was found that FIP-fve stimulated cell proliferation and enhanced IL-2 secretion in a dose-dependent manner in Jurkat E6-1 cells. Unbiased high-throughput proteomics analysis showed that 4 T cell immune activation markers including ZAP-70, CD69, CD82 and KIF23 were upregulated in response to FIP-fve treatment. Further pathway analysis indicated that MAP2K3/p38 pathway related proteins including MAP2K, p38, ELK, AATF, FOS, and JUN-B were unregulated. In addition, losmapimod (p38 inhibitor) and gossypetin (MAP2K3 inhibitor) inhibited FIP-fve enhanced cell proliferation and IL-2 release in Jurkat E6-1 cells. Our results demonstrate that FIP-fve stimulates cell proliferation and enhances IL-2 secretion through MAP2K3/ p38α activation.
2022-06-09 | PXD032302 | Pride
Project description:Gene expression in Jurkat T cell lines
| PRJNA505417 | ENA
Project description:Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has been shown to be a potent inducer of apoptosis in various cancer cell lines and primary cancer cells. However, in clinical trials administration of recombinant TRAIL or TRAIL death receptor agonists did not show sufficient efficacy for treatment of tested malignant disorders compared to standard chemotherapy. Acquired resistance of cancer cells to TRAIL and to other âdeath receptorâ ligands may explain not only the inability of TRAIL and TRAIL âdeath receptorâ agonists to achieve the clearance of cancer cells in vivo but also the escape of cancer cells from immune cell â mediated killing. Selective pressure of TRAIL on TRAIL-sensitive Jurkat T-lymphoblastic leukemia cells provided several TRAIL resistant Jurkat cell line clones (TR1, TR2, TR3). Irrespective of molecular changes histone deacetylase inhibitors (HDACi), such as suberoylanilide-hydroxamic acid (SAHA, vorinostat), were able to restore sensitivity of all three TRAIL-resistant clones to TRAIL. Gene expression analysis of TR1 clone treated with SAHA 1microM for 12 hours compared to untreated TR1 clone showed significant decrease in expression of CFLAR/cFLIP (0.71; p=0.006), BIRC5/survivin (0.80; p=0.024) and BID (0.66; p<0.001). Expression of both TRAIL âdeathâ receptors DR4 (1.57; p<0.001) and DR5 (1.47; p=0.002) were significantly increased compared to untreated TR1 cells. The mRNA expression of caspases-2,-3,-8,-9,-10 did not significantly change with the SAHA treatment. Total cellular RNA was isolated from biologic duplicates of untreated Jurkat cells (WT), TRAIL resistant Jurkat cell clone (TR1) and 1 µM and 0.5 µM suberoylanilide-hydroxamic acid (SAHA, vorinostat) treated TR1 cell clones for 12 hours. Jurkat cell line subclones TR1was established by selective pressure of TRAIL 1000 ng/mL on Jurkat cells over the period of 12 weeks.
2016-06-15 | E-GEOD-38745 | biostudies-arrayexpress