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UGT2B17 knock down in chronic lymphocytic leukemia cell line MEC-1

ABSTRACT: Comparison of gene expression after stable shRNA induced knock down of UGT2B17 and scrambled shRNA in the cell line model MEC-1. Transfection was performed using lentiviral particles, RNA was harvested after culture for 2 weeks. Results provide insight into functional UGT2B17 involvement in CLL cells. Knock down of UGT2B17 in comparison to scrambled shRNA in three independent replicates each.

ORGANISM(S): Homo sapiens

SUBMITTER: Robin Ristl

PROVIDER: E-GEOD-38367 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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UGT2B17 knock down in chronic lymphocytic leukemia cell line MEC-1

Project description:Comparison of gene expression after stable shRNA induced knock down of UGT2B17 and scrambled shRNA in the cell line model MEC-1. Transfection was performed using lentiviral particles, RNA was harvested after culture for 2 weeks. Results provide insight into functional UGT2B17 involvement in CLL cells.

2015-05-01 | GSE38367 | GEO

SLAMF1/CD150 regulates chemotaxis, autophagy and therapy responses in chronic lymphocytic leukemia patients

Project description:This work shows that signaling-lymphocytic-activation-molecule-1 (SLAMF1), a co-stimulatory molecule and a microbial sensor, is expressed by normal CD19+/CD5+ B-lymphocytes. Its expression is lost in a subset of patients with chronic lymphocytic leukemia (CLL) characterized by an aggressive form of the disease, with shorter time to first treatment and overall survival. Silencing of SLAMF1 in the CLL-like Mec-1 cell line (constitutively SLAMF1+) modulated pathways connected to cell migration, cytoskeletal organization and intracellular vesicle formation/recirculation. Loss of SLAMF1 was associated to increased expression of CXCR4, CD38 and CD44, positively affecting chemotactic responses to CXCL12. Ligation of SLAMF1 with an agonistic monoclonal antibody promoted the autophagic flux, by increasing reactive oxygen species (ROS) accumulation and inducing phosphorylation of p38, JNK1/2 and bcl-2. The direct consequence was the assembly of the autophagy macro-complex that included SLAMF1, the scaffold protein Beclin1 and the enzyme Vps34. Consistently, SLAMF1-silenced cells or SLAMF1low primary CLL cells were resistant to autophagy-activating therapeutic agents, such as fludarabine or the BH3 mimetic ABT-737. These results indicate that loss of SLAMF1 expression modulates genetic pathways regulating chemotaxis and autophagy and potentially affecting drug responses, thus providing a likely explanation for the unfavorable clinical outcome experienced by this patient subset. Microarrays were performed comparing genetic signature of CLL-like Mec-1 cell line (constitutively SLAMF1+), transfected with a non-effective (scrambled) shRNA cassette (TR30013) used as control, and a Mec-1 variant generated silencing SLAMF1 gene using pGFP-V-RS construct for SLAMF1 shRNA (TG309422). For each cell line variants, grown in vitro in complete medium, three biological replicates were included in the chip.

2015-05-23 | E-GEOD-69165 | biostudies-arrayexpress

PKCÎ´ regulates the transformed growth of K-ras dependent lung cancer cells through regulation of integrin Î±VÎ²3 expression

Project description:To explore how PKCÎ´ regulates tumorigenesis, we performed mRNA expression analysis of four KRAS mutant NSCLC cell lines that stably express scrambled shRNA or PKCÎ´ targeted shRNA Four human lung cancer cell lines (A549, H441, H460 and H2009) with scrambled and PKC-delta knock down (shRNA), in triplicate.

2016-09-01 | E-GEOD-72788 | biostudies-arrayexpress

Toll-like receptor 9 signaling in chronic lymphocytic leukemia cell lines

Project description:To investigate Toll-like receptors (TLR) signaling in Chronic lymphocytic leukemia (CLL) cell lines, we analyzed HG-3, MEC-2 and PCL-12 CLL cell lines before and after TLR9 stimulation by RNA-sequencing followed by bioinformatic analyses and validation experiments.

2023-09-19 | GSE233595 | GEO

Lipoprotein lipase in chronic lymphocytic leukemia - strong biomarker with lack of functional significance

Project description:LPL co-deregulated genes after LPL specific siRNA knock-down In chronic lymphocytic leukemia (CLL), lipoprotein lipase (LPL) mRNA overexpression is an established poor prognostic marker, its function, however, is poorly understood. Measuring extracellular LPL enzymatic activity and protein, we found no difference between levels in CLL patients and those of controls, both before and after heparin treatment in vivo and in vitro. Investigating LPL knock down effects, we determined five potential downstream targets, of which one gene, STXBP3, reportedly is involved in fatty acid metabolism. While possibly reflecting an epigenetic switch towards an incorrect transcriptional program, LPL overexpression by itself does not appear to significantly influence CLL cell survival.

2013-02-13 | E-GEOD-44247 | biostudies-arrayexpress

Effect of chronic lymphocytic leukemia-derived exosomes on human bone marrow mesenchymal stem cells

Project description:Transcription profiling of human bone marrow mesenchymal stem cells treated with exosomes isolated from chronic lymphocytic leukemia cell line MEC-1 supernatant. Cells were left untreated or treated with CLL-exosomes for 6h at 37C.

2015-06-21 | E-MTAB-2765 | biostudies-arrayexpress

Lipoprotein lipase in chronic lymphocytic leukemia - strong biomarker with lack of functional significance

2013-02-13 | GSE44247 | GEO

Identification of CRTC1-MAML2 fusion oncogene-regulated transcriptional program in H3118 cells

Project description:Mucoepidermoid carcinomas (MEC) is the most common salivary gland malignancy. To date, advanced and nonresectable MEC have poor prognosis and no effective treatment. The CRTC1-MAML2 fusion oncogene, which is associated with more than 50% of MEC, consists of the N-terminal CREB-binding domain of the CREB transcriptional co-activator CRTC1 and the C-terminal transcriptional activation domain of the Notch transcriptional co-activator MAML2. CRTC1-MAML2 fusion was found to interact with CREB and constitutively activate their transcriptional targets. To investigate the genes and pathways regulated by CRTC1-MAML2 fusion oncogene, gene expression profiling analysis were performed in human fusion-positive MEC cells before and after knockdown of both CRTC1-MAML2 and MAML2 as well as in human fusion-negative salivary gland cancer cells before and after MAML2 knockdown only. This study revealed specific transcriptional program induced by the CRTC1-MAML2 fusion oncogene, which potentially mediates CRC1-MAML2 functions in MEC initiation and maintenance. The information will be useful for developing new approaches to block CRTC1-MAML2 fusion-expressing MEC. The fusion-positive H3118 MEC cells were used in this study. The fusion knockdown was performed with two biological replicates for each group. Since we are unable to obtain any shRNA that causes specific knockdown of CRTC1-MAML2, we utilized pSuperRetro-based retroviruses that express shRNA targeting the MAML2 TAD as well as GFP for fusion knock down, and the retroviruses express shRNA targeting luciferase gene (shLuc) and GFP for the control. Cells were infected with retroviruses and cultured for 48 hours. FACS sorting was performed to obtain GFP-positive cells and thus enrich shRNA-expressing cells. RNA was subsequently harvested for microarray analysis. The shMAML2 retroviruses caused the knockdown of MAML2 and CRTC1-MAML2 fusion in fusion-positive H3118 cells.

2014-04-21 | E-GEOD-46580 | biostudies-arrayexpress

Stromal cells support the survival of human primary chronic lymphocytic leukemia (CLL) cells

Project description:In chronic lymphocytic leukemia (CLL), the tumor cells receive survival support from stromal cells through direct cell contact, soluble factors and extracellular vesicles. The tyrosine protein kinase Lyn, is aberrantly expressed in the malignant and stromal cells in CLL tissue. We therefore studied the role of Lyn in the EV-based communication and tumor support. We compared the Lyn-dependent EV release, uptake and functionality using Lyn-proficient and deficient stromal cells and primary CLL cells. Lyn-proficient cells caused a significantly higher EV release and EV uptake as compared to Lyn-deficient ones. Also, they induced stronger support of primary CLL cells. Proteomic comparison of the EVs from Lyn-proficient and deficient stromal cell highlighted 72 significantly differentially expressed proteins, many of which belonging to the extracellular matrix organization, such as collagen, nidogen, fibronectin and endosialin (CD248). CD248, a marker of certain tumors and of cancer associated fibroblast (CAF) was significantly depleted in Lyn-deficient HS-5 cells. A knockdown of CD248 in Lyn+ HS-5 cells resulted in a diminished B-CLL cells survival feeding capacity compared to wildtype or scrambled control cells. The presented data provide preclinical evidence, that the tyrosine kinase Lyn crucially influences the EV-based communication between stromal and primary B-CLL cells by raising the EV release and their concentration of functional molecules, such as endosialin.

2023-01-12 | PXD036932 | Pride

Gene knock down studies revealed CCDC50 as candidate gene in mantle cell lymphoma and chronic lymphocytic leukemia

Project description:The two B-cell non-Hodgkin lymphoma (NHL) entities chronic lymphocytic leukemia (CLL) and mantle cell lymphoma (MCL) show recurrent chromosomal gains of 3q25 q29, 12q13 q14 and 18q21-q22. The pathomechanisms affected by these aberrations are not understood. The aim of this study was to identify genes, located within these gained regions, which control cell death and cell survival of MCL and CLL cancer cells. Blood samples from 24 CLL and 6 MCL patients as well as 6 cell lines representing both malignancies were analyzed by gene expression profiling. By comparison of genomic DNA and gene expression, 72 candidate genes were identified. We performed a limited RNAi screen with these candidates in order to identify genes affecting cell survival. CCDC50, SERPINI2 and SMARCC2 mediated a reduction of cell viability in primary CLL cells as well as in cell lines. Gene knock down and a NFkB reporter gene assay revealed that CCDC50 is required for survival in MCL and CLL cells and controls NFkB signaling. This SuperSeries is composed of the SubSeries listed below.

2010-06-03 | GSE16413 | GEO

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