Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

13 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

GEP data from BCWM.1 cells treated with LNA antimiR-155 or scramble control

ABSTRACT: microRNA-155 acts as an oncogenic miRNA in B-cell lymphoproliferative disorders including Waldenstrom Macroglobulinemia (WM) and Chronic Lymphocytic Leukemia (CLL). we used an 8-mer LNA (locked nucleic acid) phosphorothioate oligonucleotide targeting the seed region of miR-155 to effectively antagonize in vitro tumor growth in WM. We performed gene expression profiling (GEP) analysis on BCWM.1 cells after treatment with LNA antimiR-155 or scramble control for 48 hours.

ORGANISM(S): Homo sapiens

SUBMITTER: Yong Zhang

PROVIDER: E-GEOD-39189 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Tetraspanin TSPAN12 regulates tumor growth and metastasis and inhibits b-catenin degedation

Project description:Ablation of tetraspanin protein TSPAN12 from human MDA-MB-231 cells resulted in a major decrease in primary tumor xenograft growth, accompanied by a significant increase in tumor apoptosis. Furthermore, TSPAN12 removal markedly increased metastasis to mouse lungs, due to enhanced tumor-endothelial interactions. Removal of TSPAN12 from human MDA-MB-231 cells also caused substantial proteosomal degradation of Î²-catenin, a key effecter of canonical Wnt signalling. This may be explained by TSPAN12 ablation leading to diminished association between FZD4 (a key receptor in the canonical Wnt pathway) and its co-receptor LRP5. Consistent with disruption of canonical Wnt signaling, TSPAN12 ablation altered the expression of LRP5, Naked 1 and 2, DVL2, DVL3, Axin 1 and GSKÎ²3 proteins, and also altered expression of several genes regulated by Î²-catenin. In conclusion, these results provide the first evidence for TSPAN12 playing a role in supporting primary tumor growth and suppressing metastasis. TSPAN12 appears to function by stabilizing FZD4-LRP5 association, in support of canonical Wnt-pathway signaling, leading to enhanced Î²-catenin expression and function. 4 samples = 2 Control + 2 TSPAN12KD

2012-10-29 | E-GEOD-41892 | biostudies-arrayexpress

GEP data from BCWM.1 cells treated with LNA antimiR-155 or scramble control

Project description:microRNA-155 acts as an oncogenic miRNA in B-cell lymphoproliferative disorders including Waldenstrom Macroglobulinemia (WM) and Chronic Lymphocytic Leukemia (CLL). we used an 8-mer LNA (locked nucleic acid) phosphorothioate oligonucleotide targeting the seed region of miR-155 to effectively antagonize in vitro tumor growth in WM.

2012-07-10 | GSE39189 | GEO

Inhibition of miR-9 regulates HuR and DICER1 and blocks Hodgkin Lymphoma tumor outgrowth

Project description:An Hodgkin Lymphoma cell line have been treated with an LNA inhibitor for miR-9 or with a scramble LNA to identify miR-9 regulated pathways that could be important for Hodgkin Lymphoma pathogenesis. L428 cells were transfected with a miR-9 LNA inhibitor or a scrambled LNA. Total RNA was harvested 9 hours post-transfection and analyzed on Affymetrix HG-U133 Plus 2.0 human arrays. A total of six arrays were analyzed. For filtering, uninformative genes with the same expression level across all arrays (including non-expressed genes) were removed and the differentially expressed genes, their corresponding p-values and false discovery rates were calculated using limma.

2012-05-01 | E-GEOD-27529 | biostudies-arrayexpress

Gene expression profiling of Down Syndrome (DS)-AMKL and non-DS AMKL samples

Project description:The goal of this study is to define a gene expression signature unique to DS-AMKL (acute megakaryoblastic leukemia or FAB M7 leukemia). A similar study was done previously, but using unfractionated patient leukemic samples. In this study, we sorted megakaryocytic leukemia blasts from patients and then compared their gene expression signatures to those from similarly sorted blasts from patients with non-DS AMKL. This allowed us to identify a gene expression signature more unique to DS-AMKL samples. The leukemic blasts were sorted based on CD41, CD7, CD117, CD33, and CD34 antibodies as previously described (Klin. Padiatr. 217, 126-134).

2010-08-01 | E-GEOD-16677 | biostudies-arrayexpress

Plag1 overexpression cooperates with Evi1 overexpression and Gata1s mutation in leading to M7 leukemia

Project description:The goal of this study is to develop a Plag1 signature and determine how its overexpression contributes to leukemogenesis. To study this, we transduced an immortalized (but not transformed) cell line (derived from Gata1s mutant fetal liver progenitor through insertional mutagenesis) by Plag1-expressing retrovirus. This turned a non-transformed cell line to a leukemogenic cell line. To study whether Plag1 overexpression led to deregulation of signaling pathways that may contribute to leukemic transformation, we generated microarray gene expression profiles of this cell line transduced with either Plag1 or the empty vector. We generated gene expression profiles by microarray from stable cell lines transduced with either the empty vector or the Plag1-expressing vector.

2010-08-01 | E-GEOD-16679 | biostudies-arrayexpress

Murine M7 leukemia derived from retroviral insertional mutagenesis of Gata1s fetal progenitors

Project description:The goal of this study is to derive a mouse model of human Down Syndrome (DS) megakaryocytic leukemia involving mutations in the hematopoietic transcription factor, GATA1 (called GATA1s mutation). We achieved this through transduction of Gata1s mutant fetal progenitors by MSCV-based retrovirus expressing a GFP marker, followed by in vitro selection (for immortalized cell lines), and then in vivo selection (for transformed cell lines) through transplantation. Here we report one such cell line [T6(6)] that gives rise to megakaryocytic leukemia (M7 leukemia) upon transplantation. Since the leukemic cells were retrovirally tagged with a GFP reporter, we sorted GFP+ leukemic blasts and generated their expression profiles by microarray.

2010-08-01 | E-GEOD-16682 | biostudies-arrayexpress

Developmental stage-specific interplay between GATA1 and IGF signaling in fetal hematopoiesis and leukemogenesis

Project description:This SuperSeries is composed of the following subset Series: GSE16676: Rescue of murine Gata1s mutant M7 leukemic cells by full-length Gata1 GSE16677: Gene expression profiling of Down Syndrome (DS)-AMKL and non-DS AMKL samples GSE16679: Plag1 overexpression cooperates with Evi1 overexpression and Gata1s mutation in leading to M7 leukemia GSE16682: Murine M7 leukemia derived from retroviral insertional mutagenesis of Gata1s fetal progenitors GSE16684: Murine M7 leukemia derived from retroviral insertional mutagenesis of Gata1s fetal progenitors depends on IGF signaling Refer to individual Series

2010-08-01 | E-GEOD-16655 | biostudies-arrayexpress

Murine M7 leukemia derived from retroviral insertional mutagenesis of Gata1s fetal progenitors depends on IGF signaling

Project description:The goal of this study is to derive a mouse model of human Down Syndrome (DS) megakaryocytic leukemia involving mutations in the hematopoietic transcription factor, GATA1 (called GATA1s mutation). We achieved this through transduction of Gata1s mutant fetal progenitors by MSCV-based retrovirus expressing a GFP marker, followed by in vitro selection (for immortalized cell lines), and then in vivo selection (for transformed cell lines) through transplantation. Here we report one such cell line [T6(6)] that gives rise to megakaryocytic leukemia (M7 leukemia) upon transplantation. We show knockdown of IGF1R in these cells leads to their reduced proliferation. IGF1R was knocked down in these cells using a tet-regulatable shRNA-based lentiviral system. Cells infected with the empty vector or those infected with shRNA construct against IGF1R but in the absence of Doxycycline were used as controls. The latter cells in the presence of Doxycycline exhibited reduced IGF1R at the RNA level.

2010-08-01 | E-GEOD-16684 | biostudies-arrayexpress

Rescue of murine Gata1s mutant M7 leukemic cells by full-length Gata1

Project description:In this project, we studied a mouse model of human Down Syndrome (DS) megakaryocytic leukemia involving mutations in the GATA1 transcription factor (called GATA1s mutation). The model was generated through retroviral insertional mutagenesis in Gata1s mutant fetal liver progenitors. In this study, we analyzed the dependency of these leukemic cells on the Gata1s mutant protein. Here we report Gata1s mutant leukemic cells were dependent on this mutant protein. Introduction of the full-length Gata1 protein to these cells led to their reduced proliferation and increased differentiation along the megakaryocytic lineage. We transduced leukemic cells with Gata1/estrogen receptor fusion cDNA (Gata1-ER) and generated stable cell lines. Addition of beta-estradiol to culture medium led to activation of the full-length Gata1 protein in synchronized leukemic cells. Gene expression profiles were collected at multiple time points.

2010-08-01 | E-GEOD-16676 | biostudies-arrayexpress

Identification differentially expressed genes upon valproic acid treatment

Project description:The goal of this study is to define genes that are differentially expressed in Down syndrome leukemic blasts after treatment with valproic acid (VPA) Here we report the identification gene sets that are downregulated in Down syndrome leukemic cell lines after exposure to valproic acid (VPA) CMK and CMY cells were treated with VPA for 24h and 48h with 1mM or 2mM VPA. Their gene expression profile was compared against the untreated control.

2011-07-12 | E-GEOD-30517 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data