Genome-wide identification of genes directly regualted by GFI1 and IKAROS in CCRF-CEM cells
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ABSTRACT:
PROVIDER: PRJNA672151 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12903453.fastq.gz | Fastqsanger.gz | |||
| SRR12903454.fastq.gz | Fastqsanger.gz | |||
| SRR12903455.fastq.gz | Fastqsanger.gz | |||
| SRR12903456.fastq.gz | Fastqsanger.gz | |||
| SRR12903457.fastq.gz | Fastqsanger.gz |
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Project description:To study the interplay between GFI1 and IKAROS in T-cell Acute Lymphoblastic Leukemia (T-ALL), we applied ChIP-Seq to CCRF-CEM cells expressing 3XFLAG-tagged GFI1 OR IKAROS under doxycycline-inducible control.We found these two protiens associated with common genes, including genes associated with T cell development.
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Project description:To identify changes in gene expression associated with either ectopic GFI1 expression or CRISPR-mediated IKAROS knockout, we applied bulk RNA-Seq with GFI1-3XFLAG CCRF-CEM cells. Wild type or IKAROS knockout cells were treated with vehicle or doxycycline for 24 hours. Between 21.7 and 28.2 million RNA-Seq reads were generated for each condition, 88.6 to 90.3% of which aligned uniquely to the human Hg38 reference genome. ~99% of the reads within coding regions aligned to the correct strand. Hierarchically clustering the top 500 most significantly differentially regulated genes across all the conditions (ranked based on p-value) revealed groups of genes repressed and activated by the different manipulations.
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Project description:Bortezomib is a proteasome inhibitor used in severel different hematological malignancies. Resistance to this drug is still poorly understood. In order get more insight in the resistance mechanism, we developed several bortezomib resistant subclones of the CCRF-CEM T-ALL cell line. On these subclones comparative Genome hybridization (arrayCGH) for DNA copy number analysis gene expression and micro-RNA expression arrays were performed. We performed micro-RNA on two different bortezomib resistant subclones of the CCRF-CEM cell line. The resistant subclones were compared to the parental CCRF-CEM wildtype cell line.
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Project description:Bortezomib is a proteasome inhibitor used in severel different hematological malignancies. Resistance to this drug is still poorly understood. In order get more insight in the resistance mechanism, we developed several bortezomib resistant subclones of the CCRF-CEM T-ALL cell line. On these subclones comparative Genome hybridization (arrayCGH) for DNA copy number analysis gene expression and micro-RNA expression arrays were performed. We performed comparative Genome hybridization (arrayCGH) for DNA copy number analysis on four different bortezomib resistant subclones of the CCRF-CEM cell line. The resistant subclones were compared to the parental CCRF-CEM wildtype cell line and reference DNA.
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Project description:Bortezomib is a proteasome inhibitor used in severel different hematological malignancies. Resistance to this drug is still poorly understood. In order get more insight in the resistance mechanism, we developed several bortezomib resistant subclones of the CCRF-CEM T-ALL cell line. On these subclones comparative Genome hybridization (arrayCGH) for DNA copy number analysis gene expression and micro-RNA expression arrays were performed. We performed gene expression microarray analysis on four different bortezomib resistant subclones of the CCRF-CEM cell line. The resistant subclones were compaired to treated and untreated the parental CCRF-CEM wildtype cell line.
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Project description:It has been shown previously that glucocorticoids exert a dual mechanism of action, entailing cytotoxic, mitogenic as well as cell proliferative and anti-apoptotic responses, in a dose-dependent manner on CCRF-CEM cells at 72 h. Early gene expression response implies a dose-dependent dual mechanism of action of prednisolone too, something reflected on cell state upon 72 h of treatment. In this work, a generic, computational microarray data analysis framework is proposed, in order to examine the hypothesis whether CCRF-CEM cells exhibit an intrinsic or acquired mechanism of resistance and to investigate the molecular imprint of this, upon prednisolone treatment. The experimental design enables the examination of both the dose (0 nM, 10 nM, 22 uΜ, 700 uΜ) effect of glucocorticoid exposure and the dynamics (early and late, namely 4 h, 72 h) of the molecular response of the cells at the transcriptomic layer. In this work we demonstrated that CCRF-CEM cells may attain a mixed mechanism of response to glucocorticoids, however, there is clear evidence predicating towards an intrinsic mechanism of resistance. More specifically, at 4 h prednisolone appeared not to perform its expected function by down-regulating apoptotic genes, which is re-enforced by mechanisms, which down-regulate other sets of apoptotic genes. Also, low and high prednisolone concentrations up-regulates metabolic and signal-transduction related genes in both time points, thus grounding for a cell proliferation machinery. In addition, regulation of NF-κB-related genes implies an inherent mechanism of resistance through the established link of NF-κB inflammatory role and GC-induced resistance. The analysis framework applied here allows derivation of regulatory mechanisms activated by prednisolone through identification of early responding sets of genes. On the other hand, study of the prolonged exposure to glucocorticoids (72 h exposure) highlights the effect of homeostatic feedback mechanisms of the treated cells. Overall, it appears that CCRF-CEM cells in this study exhibit a diversified, combined pattern of intrinsic and acquired resistance to prednisolone, yet with a tendency towards inherent resistant characteristics, through activation of different molecular courses of action.
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Project description:Bortezomib is a proteasome inhibitor used in severel different hematological malignancies. Resistance to this drug is still poorly understood. In order get more insight in the resistance mechanism, we developed several bortezomib resistant subclones of the CCRF-CEM T-ALL cell line. On these subclones comparative Genome hybridization (arrayCGH) for DNA copy number analysis gene expression and micro-RNA expression arrays were performed.
2015-11-04 | GSE74632 | GEO
Project description:Bortezomib is a proteasome inhibitor used in severel different hematological malignancies. Resistance to this drug is still poorly understood. In order get more insight in the resistance mechanism, we developed several bortezomib resistant subclones of the CCRF-CEM T-ALL cell line. On these subclones comparative Genome hybridization (arrayCGH) for DNA copy number analysis gene expression and micro-RNA expression arrays were performed.
2015-11-04 | GSE74633 | GEO