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Gene expression changes induced by the pan-PIM inhibitor ETP-39010 in 4 peripheral T cell lymphoma cell lines

ABSTRACT: Peripheral T cell lymphoma (PTCL) is a very aggressive disease which currently lacks efficient targeted therapy. New therapeutic strategies are needed to improve the very poor outcome of these patients. In these study we hypothesized that PIM kinases could be of therapeutic value in PTCL because we found an overexpression of PIM1 and PIM2, but not PIM3, in PTCL cases, cell lines and primary tumoral T cells from Sezary Syndrome patients, compared with reactive lymph nodes and normal T cells from healthy donors, respectively. In order to understand the mechanism of action of this pan-PIM inhibitor in PTCL, 4 cell lines (DERL7, HuT78, SR786 and MyLa) were treated with 10 μM of ETP-39010 for 0, 2, 4, 6, 10 and 24 h, and gene expression profiling was performed.

ORGANISM(S): Homo sapiens

PROVIDER: GSE42595 | GEO | 2014/11/14

SECONDARY ACCESSION(S): PRJNA182327

REPOSITORIES: GEO

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Gene expression changes induced by the pan-PIM inhibitor ETP-39010 in 4 peripheral T cell lymphoma cell lines

Project description:Peripheral T cell lymphoma (PTCL) is a very aggressive disease which currently lacks efficient targeted therapy. New therapeutic strategies are needed to improve the very poor outcome of these patients. In these study we hypothesized that PIM kinases could be of therapeutic value in PTCL because we found an overexpression of PIM1 and PIM2, but not PIM3, in PTCL cases, cell lines and primary tumoral T cells from Sezary Syndrome patients, compared with reactive lymph nodes and normal T cells from healthy donors, respectively. In order to understand the mechanism of action of this pan-PIM inhibitor in PTCL, 4 cell lines (DERL7, HuT78, SR786 and MyLa) were treated with 10 Î¼M of ETP-39010 for 0, 2, 4, 6, 10 and 24 h, and gene expression profiling was performed. 4 PTCL cell lines (DERL7, HuT78, SR786 and MyLa) were treated with DMSO and 10 Î¼M of the pan-PIM inhibitor ETP-39010, and hybridized using the Universal Human Reference RNA (Stratagene, La Jolla, CA) as the reference sample.

2014-11-14 | E-GEOD-42595 | biostudies-arrayexpress

Proviral integration site for Moloney murine leukemia virus (PIM) kinases promote human T helper 1 cell differentiation

Project description:The aim of the dataset was to study on genome-wide level the effect of PIM kinase (PIM1+PIM2+PIM3) knockdown in gene expression on early differentiation of human cord blood derived CD4+ T cells cultured under Th1 (Act+IL12) polarizing conditions. Total RNA from PIM1+PIM2+PIM3 siRNA treated cord blood CD4+ T cells 6 hours after culturing the cells in activating (antiCD3+antiCD28) plus IL-12 (Th1) or IL-4 (Th2) conditions was compared to total RNA from nonspecific control siRNA treated cells. Samples from 3 biological replicates were analysed.

2012-12-05 | E-GEOD-40542 | biostudies-arrayexpress

Proviral integration site for Moloney murine leukemia virus (PIM) kinases promote human T helper 1 cell differentiation

2012-12-05 | GSE40542 | GEO

Monocyte-derived dendritic cells response to mycobacterial glycolipid, phosphatidyl-inositol mannosides (PIM)

Project description:Phosphatidyl-inositol mannosides (PIM) are unique mycobacterial glycolipids. However, the PIM-induced immunostimulatory activities remain controversial. Here we report on gene expression analysis of monocyte-derived dendritic cells stimulated with tri-acylated PIM2 (AcPIM2) or tetra-acylated PIM2 (Ac2PIM2). Results provide evidence for the adjuvant activity of PIM.

2017-01-31 | GSE84740 | GEO

Transcriptome of SATB1 transduced Hut78 cells

Project description:Hut78 cell line was used as Sezary syndrome cell model. Comparative transcriptome profiles of SATB1 transduced Hut78 cells (Hut78-SATB1) relative to empty MIG vector transduced control Hut78 cells (Hut78-MIG) were analyzed. The primary goal is to establish a list of genes with differential expression between SATB1 transduced Hut78 cells and control Hut78 cells to identify the gene expression regulation effect of SATB1 expression in Sezary cells.

2011-12-01 | GSE24951 | GEO

Transcriptome of SATB1 transduced Hut78 cells

2011-12-01 | E-GEOD-24951 | biostudies-arrayexpress

Whole Proteomics of 24 hr pan Pim kinase inhibitor treatment of IL2 cultured CD8 T cells

Project description:T cell antigen-receptor (TCR) and cytokine receptor engagement trigger large changes in Serine/Threonine kinase signalling networks to drive T cell activation and differentiation. The role of only few kinase signalling pathways have been studied in detail, and in this context, Pim kinases are an interesting, yet understudied, family of Serine/Threonine kinases, with reported roles in key processes including survival, proliferation, metabolism across a range of cell types. T lymphocytes predominantly express PIM1 and PIM2, which are rapidly induced by TCR, costimulation and cytokine signalling. Using single shot DDA mass spectrometry we examine the impact of 24 hours treatment with two different pan-Pim kinase inhibitors PIM447 and AZD1208 on in vitro IL2 differentiated effector cytotoxic T lymphocytes. The Jak1/3 inhibitor tofacitinib was included as a control as this also blocks production of Pim kinases downstream of IL2. We find that treatment with pan-Pim kinase inhibitors has a similar phenotype to Pim1/Pim2 double deficiency, showing a reduction in proteins that are key for effector cell function: glucose transporters SLC2A1 and SLC2A3 and key effector molecule Granzyme B and an increase in the translational repressor PDCD4.

2024-04-15 | PXD051214 | Pride

Transcriptome Signatures of Sezary Cells from Patients and Cultured Hut 78, Hut 102 and Jurkat Cells

Project description:Comparative transcriptome profiles of patient-derived Sezary cells and cultured Sezary cell line (Hut78) mycosis fungoides cell line (Hut 102) and non-Sezary T cell leukemia cell line (Jurkat) relative to benign CD4+ T cells from individuals with no T cell malignancy. There are three goals. The first and primary goal is to establish a list of genes with differential expression between Sezary cells and the benign CD4+ T cell counter part from individuals without Sezary syndrome. A secondary goal is to examine if these differentially expresses genes in clinical samples of Sezary cells are preserved in Hut78 and Hut102 cells, which are the two most frequently used experimental cell models of Sezary cells in the research community. The third goal is to examine if these Sezary cell specific genes are also present in a non-Sezary T cell malignancy, such as Jurkat cells, which is derived from a non-Sezary cell T cell leukemia patient. Two color experiment, 6 biological replicates (6 unique patients) with Sezary syndrome, 1 Hut78 cell,1 Hut102 cell and 1 Jurkat cell lines as the experimental samples, each compared with a distinct individual with no T cell malignancy of the skin or the blood.

2010-12-31 | E-GEOD-23113 | biostudies-arrayexpress

Gene-expression profile in a series of non-Hodgkin lymphoma (NHL) patients

Project description:PIM serine/threonine kinases are overexpressed, translocated or amplified in multiple B-cell lymphoma types. We have explored the frequency and relevance of PIM expression in different B-cell lymphoma types, and investigated whether PIM inhibition could be a rational therapeutic approach. Increased expression of PIM2 was detected in subsets of mantle cell lymphoma (MCL), diffuse large B-cell lymphoma (DLBLC), follicular lymphoma (FL), marginal zone lymphoma-MALT type (MZL-MALT), chronic lymphocytic leukemia (CLL) and nodal marginal zone lymphoma (NMZL) cases. Increased PIM2 protein expression was associated with an aggressive clinical course in ABC-DLBCL patients. Pharmacological and genetic inhibition of PIM2 revealed p4E-BP1(Thr37/46) and p4E-BP1(Ser65) as molecular biomarkers characteristic of PIM2 activity, and indicated the involvement of PIM2 kinase in regulating mTORC1. The simultaneous genetic inhibition of all three PIM kinases induced changes in apoptosis and cell cycle. In conclusion, we show that PIM2 kinase inhibition is a rational approach in DLBCL treatment, identify appropriate biomarkers for pharmacodynamic studies, and provide a new marker for patient stratification. Gene-expression profiling was conducted in a series of 114 B-cell non-Hodgkin lymphoma patients (DLBCL, FL, MALT, MCL, CLL and NMZL). Seven freshly frozen lymph nodes and six freshly frozen reactive tonsils were used as controls.

2011-10-16 | E-GEOD-32018 | biostudies-arrayexpress

Gene-expression profile in a series of non-Hodgkin lymphoma (NHL) patients

2011-10-17 | GSE32018 | GEO

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