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Whole genome gene expression profiling in Adult T-cell Leukemia (ATL) cells and in Normal CD4+ T-cells

ABSTRACT: HTLV-1 infected individuals stay as carriers for their lifetimes, while the rest of 5% are killed by ATL. ATL leukemogenesis is a complex process involving accumulation of multiple genetic abnormalities in HTLV-1 infected cells. To clarify genetic events underlying ATL leukemogenesis, we conducted comprehensive gene expression profiling in 52 ATL patients and in 21 healthy volunteers. Total RNA samples from PBMC of ATL patients (mostly HTLV-1 inefcted CD4+ T-cells) and from CD4+ T-cells from healthy donors were subjected to Cy-3 labeling followed by human whole genome gene expression microarray analyses.

ORGANISM(S): Homo sapiens

SUBMITTER: Kazumi Nakano

PROVIDER: E-GEOD-33615 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Polycomb-mediated loss of miR-31 activates NIK-dependent NF-κB pathway in adult T cell leukemia and other cancers.

Yamagishi Makoto M Nakano Kazumi K Miyake Ariko A Yamochi Tadanori T Kagami Yayoi Y Tsutsumi Akihisa A Matsuda Yuka Y Sato-Otsubo Aiko A Muto Satsuki S Utsunomiya Atae A Yamaguchi Kazunari K Uchimaru Kaoru K Ogawa Seishi S Watanabe Toshiki T

Cancer cell 20120101 1

Constitutive NF-κB activation has causative roles in adult T cell leukemia (ATL) caused by HTLV-1 and other cancers. Here, we report a pathway involving Polycomb-mediated miRNA silencing and NF-κB activation. We determine the miRNA signatures and reveal miR-31 loss in primary ATL cells. MiR-31 negatively regulates the noncanonical NF-κB pathway by targeting NF-κB inducing kinase (NIK). Loss of miR-31 therefore triggers oncogenic signaling. In ATL cells, miR-31 level is epigenetically regulated, ...[more]

PMID: 22264793

Similar Datasets

miRNA expression profiling in Adult T-cell Leukemia (ATL) cells and in Normal CD4+ T-cells

Project description:HTLV-1 infected individuals stay as carriers for their lifetimes, while the rest of 5% are killed by ATL. ATL leukemogenesis is a complex process involving accumulation of multiple genetic abnormalities in HTLV-1 infected cells. To clarify genetic events underlying ATL leukemogenesis, we conducted comprehensive miRNA expression profiling in 40 ATL patients and in 22 healthy volunteers. Total RNA samples from PBMC of ATL patients (mostly HTLV-1 inefcted CD4+ T-cells) and from CD4+ T-cells from healthy donors were subjected to Cy-3 labeling followed by miRNA expression microarray analyses.

2012-02-23 | E-GEOD-31629 | biostudies-arrayexpress

miRNA expression profiling in Adult T-cell Leukemia (ATL) cells and in Normal CD4+ T-cells

2012-02-23 | GSE31629 | GEO

Whole genome gene expression profiling in Adult T-cell Leukemia (ATL) cells and in Normal CD4+ T-cells

2012-02-23 | GSE33615 | GEO

Whole genome gene expression profiling in CD4+ T-cells, FACS-sorted based on CADM1/CD7 expression levels, in Adult T-cell Leukemia-lymphoma (ATL) patients, HTLV-1 carriers, and in healthy volunteers.

Project description:CADM1 overexpresion and stepwise downregulation of CD7 in CD4+T-cells from ATL patients and HTLV-1 carriers accurately reflect the process of disease, i.e., oligoclonally and clonally exanding cells are accumulated in D (CADM1posCD7dim) and N (CADM1posCD7neg) populations, respectively. Moreover, gene expression profiling of each subpopulation supported that notion. PBMCs of asymptomatic carriers (ACs) and ATLs were subgrouped based on CADM1 and CD7 expression levels by multicolor flow cytometry. FACS-sorted subpopulations were then subjected to extraction of total RNA, followed by Cy-3 labeling and human whole genome gene expression microarray analyses.

2014-06-02 | E-GEOD-55851 | biostudies-arrayexpress

Gene expression profiling in patients infected with HTLV-1: Identification of ATL and HAM/TSP-specific genetic profiles

Project description:We examined the gene expression profiles of CD4+ T-cells isolated from 7 ATL, 12 HAM/TSP and 11 AC (asymptomatic carriers) to identify gene signatures that may be characteristic for these particular diseases. Using gene expression arrays, we identified ~ 1039 immune-related genes that were differentially expressed in CD4+ T cells; using stringent exclusion criteria, a 122 gene signature could be divided into 3 groups: I) ATL-specific; II) common; and III) HAM/TSP-specific markers To better understand the genetic differences between HTLV-1-associated diseases, we examined the gene expression profile of T lymphocytes from patients either suffering from ATL, HAM/TSP or carrying the HTLV-1 virus without any symptoms. Microarray experiments were performed using the human ImmuneArray cDNA array (UHN Microarray Center, University of Toronto). We used the Stratagene Universal Control, labelled Cy5 for all samples in a competitive hybridization.

2010-02-13 | E-GEOD-19080 | biostudies-arrayexpress

Expression data from CD4-positive HTLV-positive cell lines and from CD4-positive HTLV-negative primary cells.

2009-08-20 | GSE17718 | GEO

KDR-dependent tyrosine phosphorylation in HTLV-1 transformed cells

Project description:Human T-cell leukemia virus type 1 (HTLV-1) is linked to the development of adult T-cell leukemia (ATL) and the neuroinflammatory disease, HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). The HTLV-1 Tax oncoprotein regulates viral gene expression and the NF-kB pathway to promote the survival of HTLV-1 infected T cells. In thsi study, we utilize a kinome-wide shRNA screen to identify the tyrosine kinase KDR/VEGFR2 as an essential survival factor of HTLV-1-transformed T cells. Inhibition of KDR induces apoptosis of Tax expressing HTLV-1-transformed cell lines and CD4+ T cells from HAM/TSP patients. Phosphoproteomics analysis of HTLV-1 transformed cells treated with a KDR inhibitor revealed inhibition of the phosphorylation of multiple receptors/cell surface proteins, ubiquitin conjugating systems, proteases, phosphatases, apoptotic regulatory factors, adhesion/extracellular matrix proteins and viral proteins. This work suggests that HTLV-1 Tax has hijacked KDR kinase activity to promote Tax stability and the proliferation and survival of HTLV-1 infected cells.

2024-06-14 | PXD051981 | Pride

Influence of ATL-type Helios overexpression or WT-Helios/Ikaros knockdown on gene expression profile in Jurkat cells

Project description:It has been known that aberrant isoforms of Ikaros family ptoteins are expressed in malignant cells. We identified that PBMC of ATL (acute T-cell leukemia) patients expresses different patterns of Helios isoforms compared with normal PBMC. In order to investigate the biological impact of ATL-type Helios isoform, we conducted complehensive gene expression analyses in Jurkat cells overexpressing ATL-type Helios. Also, we investigated the influence of WT-Helios or WT-Ikaros knockdown on the gene expression profile and compared with that of the cells with ATL-type Helios overexpression. Total RNA samples from Jurkat cells were subjected to Cy-3 labeling followed by human whole genome gene expression microarray analyses.

2013-03-31 | E-GEOD-41796 | biostudies-arrayexpress

Expression data from CD4-positive HTLV-positive cell lines and from CD4-positive HTLV-negative primary cells.

Project description:We used microarrays to compare the global programme of gene expression in HTLV-positive, ATL-derived and HTLV-positive in vitro-transformed cell lines with that of uninfected primary CD4 T cells. Cells were harvested one day after splitting, in case of primary T cells, cells were harvested after reaching a postmitotic state.

2009-08-20 | E-GEOD-17718 | biostudies-arrayexpress

DNA demethylating agents and EZH2 inhibitors for Adult T cell leukemia [Illumina]

Project description:Adult T-cell leukemia/lymphoma (ATL) is a malignancy of mature CD4+ T-cells caused by human T-cell lymphotropic virus type 1 (HTLV-1). Recently, it has been noted that some epigenome abnormalities including DNA methylation and tri-methylation at histone H3Lys27 (H3K27me3) contribute to malignant transformation of ATL. Hence, we investigate the combined effect of DNA demethylating agents and enhancer of zeste homolog 2 (EZH2), which catalyze H3K27me3, inhibitors in ATL. Methylaome analyse revealed that OR21 and the combination changes DNA methylation.

2023-05-03 | GSE189602 | GEO

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