Project description:RNA-seq analysis was performed in a T-cell acute lymphoblastic leukemia cell line (Jurkat) to analyze gene expression changes after ALDH1A2 depletion.
Project description:Several cyclin-dependent kinases (CDKs) are known to have roles in transcriptional regulation. The datasets presented here are ChIP-seq experiments for different CDKs and RNA polymerase II in murine embryonic stem cells and Jurkat cells. ChIP-Seq of cyclin-dependent kinases in mouse embryonic stem cells and Jurkat human T cell acute lymphoblastic leukemia cell line
Project description:In this research, we use DNA microarray analysis to clarify the gene expression responses in Jurkat cells after Tamoxifen treatment. Jurkat cells are a dexamethasone-resistant cell line derived from a T-cell Acute Lymphoblastic Leukaemia sample in relapse
Project description:In our efforts to evaluate the function of the IL-8 receptor CXCR2 in Acute Lymphoblastic Leukemia (ALL) cells, we made use of SB225002 (N-(2-hydroxy-4-nitrophenyl)-N’-(2-bromophenyl)urea), a drug initially described as a CXCR2 antagonist. Although the CXCR2 receptor was found to be non-functional in ALL, B- and T-ALL cell lines were sensitive to SB225002. We used microarray analysis to identify a transcriptional profile of genes that mediate SB225002's effects in acute lymphoblastic leukemia cells. Jurkat cells were treated for 6h or 9h with SB225002 [12.5 uM] or 0.1% DMSO (vehicle control).
Project description:ChIP-seq analysis was performed in a Jurkat cell line to analyze DNA bindings of TAL1-FKBP12 protein using an anti-HA antibody after DMSO or dTAG-13 treatment.
Project description:Altered metabolism is increasingly acknowledged as an important aspect of cancer, and thus serves as a potentially fertile area for the identification of therapeutic targets or leads. Our recent work using transcriptional data to predict metabolite levels in cancer cells led to preliminary evidence of the antiproliferative role of menaquinone (vitamin K2) in the Jurkat cell line model of acute lymphoblastic leukemia. However, nothing is known about the direct metabolic impacts of menaquinone in cancer, which could provide insights into its mechanism of action. Here, we used metabolomics to investigate the process by which menaquinone exerts antiproliferative activity on Jurkat cells. We first validated the dose-dependent, semi-selective, pro-apoptotic activity of menaquinone treatment on Jurkat cells relative to non-cancerous lymphoblasts. We then used mass spectrometry-based metabolomics to identify systems-scale changes in metabolic dynamics that are distinct from changes induced in noncancerous cells or by other chemotherapeutics. One of the most significantly affected metabolites was phosphoethanolamine, which exhibited a two-fold increase in menaquinone-treated Jurkat cells compared to vehicle-treated cells at 24 h, growing to a five-fold increase at 72 h. Phosphoethanolamine elevation was observed prior to the induction of apoptosis, and was not observed in menaquinonetreated lymphoblasts or chemotherapeutic-treated Jurkat cells. We also validated the link between menaquinone and phosphoethanolamine in an ovarian cancer cell line, suggesting potentially broad applicability of their relationship. This metabolomics-based work is the first detailed characterization of the metabolic impacts of menaquinone treatment and the first identified link between phosphoethanolamine and menaquinone-induced apoptosis.
Project description:RNA-seq analysis was performed in two T-cell acute lymphoblastic leukemia (T-ALL) cell lines (Jurkat and DND-41) to analyze gene expression changes after the treatment with PIK-75.
Project description:To study the effect of PPM1A-AS on T-cell acute lymphoblastic leukemia (T-ALL) cells, we conducted shRNA-mediated knockdown of PPM1A-AS in Jurkat and performed RNA-seq.