Project description:miRNA microarray expression analysis of human acute myeloid leukemia cell line (U937) after HDAC2 genetically and enzymatically defection
Project description:Alterations of TWIST-1 expression are often seen in solid tumors and contribute to tumorigenesis and cancer progression. However, studies concerning its pathogenic role in leukemia are scarce. Here we show that TWIST-1 is a new candidate gene contributing to leukemogenesis of myeloid leukemia. We used array as one tool to determine gene expression profiles of control and TWIST-1-overexpressing U937 cells.
Project description:Acute myeloid leukemia (AML) and acute T-lymphoblastic leukemia (T-ALL) maintain the undifferentiated phenotype and proliferative capacity of their respective cells of origin, hematopoietic stem/progenitor cells and immature thymocytes. The mechanisms that maintain these progenitor-like characteristics are poorly understood. We report that transcription factor Zfx is required for the development and propagation of experimental AML caused by MLL-AF9 fusion, and of T-ALL caused by Notch1 activation. In both leukemia types, Zfx activated progenitor-associated gene expression programs and prevented differentiation. Key Zfx target genes included mitochondrial enzymes Ptpmt1 and Idh2, whose overexpression partially rescued the propagation of Zfx-deficient AML. These studies identify a common mechanism that controls the cell-of-origin characteristics of acute leukemias derived from disparate lineages and transformation mechanisms. Analysis of genomic ZFX binding in the AML cell line NOMO-1 and the T-ALL cell line RPMI-8402
Project description:Validation of a custom low density microarray. Gene expression differences were analysed in the following groups of blood samples and cell lines:<br>Two haematological neoplasia cell lines: U937 (promonocytic lymphoma) versus Jurkat (T leukemia).<br>Different types of haematological neoplasias: healthy donors, B-CLL patients, myeloid leukemia patients and U937 and Jurkat cell cultures samples.<br>Two hematological neoplasia with different origin (lymphoid for B-CLL and myeloid for the myeloid group).<br>Two types of myeloid leukemias (Acute myeloid leukemia and myelodisplastic syndrome).<br>B-CLL patients with different clinical behaviour.<br>Healthy donors and B-CLL patients.<br><br>Normalization was performed using two different methods, robust quantile normalization (QRN) and variance stabilization normalization (VSN), so that a set of statistcially significant probes found using both methods could be obtained.
Project description:To investigate the molecular mechanism of matrine's anti-myeloid leukemia effect, Acute myeloid leukemia cells HL-60 and U937 and chronic myeloid leukemia cells K562 were treated with 0.8mg/mL matrine for 30min and 24h, respectively. Then, RNA-Seq data before and after matrine treatment were used for gene expression profile analysis
Project description:Approximately 20% of Acute Myelogenous Leukemia (AML) cases carry the t(8;21) translocation, which involves the AML1 and ETO genes, and express the resulting AML1/ETO fusion protein that functions as a transcriptional repressor by recruiting NCoR/SMRT/HDAC complexes to DNA. We used ChIP-chip to identify the determinants of AML1/ETO binding on a contiguous DNA region (chromosome 19). In order to correlate transcription factor binding to gene expression, we evaluated expression levels of genes localized on chromosome 19 by expression tiling. Keywords: Gene expression A U937 cell line that conditionally expresses HA-tagged AML1/ETO under the control of the mouse metallothionine promoter (U937-A1E) (Alcalay et al., J.Clin.Invest, 2003,112, 1751-1761) was used. A cell line carrying the empty vector was used as control. Cell lines were treated for 8h with 100uM ZnSO4 to induce transgene expression in U937-A1E. For each of the U937 cell lines (AML1/ETO and Mt), three independent RNA extractions were performed, and an equal quantity of each of the three RNA preparations was then mixed to generate an RNA pool for each sample.
Project description:Lhx2 is a LIM-homeobox transcription factor which could induce hematopoietic stem cell-like cells from mouse embryonic stem cells and induced pluripotent stem cells. However, the effects of Lhx2 overexpression in the human chronic myeloid leukemia cell line K562 remains unknown. Therefore we carried out Lhx2 overexpression in K562 cells.
Project description:RNA-seq was used to determine the differentially expressed genes after overexpression of two human Follistatin (FST) isoforms, FST317 and FST344 in human acute myeloid leukemia cell line ML-2.